Fish immune responses to experimental and natural infection with helminth parasites

Selected features of the responses by fish to helminth parasites are discussed and comparison is made where appropriate with mammals. These include: (i) Factors influencing host specificity and consideration of the mechanisms that underpin the restriction of some parasites in their host spectrum, (ii) How fish leucocytes kill helminth larvae, with emphasis on the role of released oxygen (ROS) and nitrogen (RNS) free radicals from macrophages, (iii) Immune evasion strategies used by fish helminths, including invasion of immunologically privileged sites, encystment, adsorption of host proteins on the parasite surface, and high surface membrane turnover, (iv) Potential immunogens for vaccination and use for immunodiagnosis of infection, and (v) Natural and induced protection against helminths, with emphasis on the potential for future vaccination strategies.     

Modulation of innate immune responses by Yersinia type III secretion system translocators and effectors

The innate immune system of mammals responds to microbial infection through detection of conserved molecular determinants called ‘pathogen‐associated molecular patterns’ (PAMPs). Pathogens use virulence factors to counteract PAMP‐directed responses. The innate immune system can in turn recognize signals generated by virulence factors, allowing for a heightened response to dangerous pathogens. Many Gram‐negative bacterial pathogens encode type III secretion systems (T3SSs) that translocate effector proteins, subvert PAMP‐directed responses and are critical for infection. A plasmid‐encoded T3SS in the human‐pathogenic Yersinia species translocates seven effectors into infected host cells. Delivery of effectors by the T3SS requires plasma membrane insertion of two translocators, which are thought to form a channel called a translocon. Studies of the Yersinia T3SS have provided key advances in our understanding of how innate immune responses are generated by perturbations in plasma membrane and other signals that result from translocon insertion. Additionally, studies in this system revealed that effectors function to inhibit innateimmune responses resulting from insertion of translocons into plasma membrane. Here, we review these advances with the goal of providing insight into how a T3SS can activate and inhibit innate immune responses, allowing a virulent pathogen to bypass host defences.     

SHARPIN is a key regulator of immune and inflammatory responses

Mice with spontaneous mutations in the Sharpin gene develop chronic proliferative dermatitis that is characterized by eosinophilic inflammation of the skin and other organs with increased expression of type 2 cytokines and dysregulated development of lymphoid tissues. The mutant mice share phenotypic features with human hypereosinophilic syndromes. The biological function of SHARPIN and how its absence leads to such a complex inflammatory phenotype in mice are poorly understood. However, recent studies identified SHARPIN as a novel modulator of immune and inflammatory responses. The emerging mechanistic model suggests that SHARPIN functions as an important adaptor component of the linear ubiquitin chain assembly complex that modulates activation of NF-κB signalling pathway, thereby regulating cell survival and apoptosis, cytokine production and development of lymphoid tissues. In this review, we will summarize the current understanding of the ubiquitin-dependent regulatory mechanisms involved in NF-κB signalling, and incorporate the recently obtained molecular insights of SHARPIN into this pathway. Recent studies identified SHARPIN as an inhibitor of β1-integrin activation and signalling, and this may be another mechanism by which SHARPIN regulates inflammation. Furthermore, the disrupted lymphoid organogenesis in SHARPIN-deficient mice suggests that SHARPIN-mediated NF-κB regulation is important for de novo development of lymphoid tissues.     

CCR4 is a key modulator of innate immune responses

CCR4 is recognized as a key receptor in Th2-associated immune processes, although very little is known about its role in innate immunity. Previous studies reported increased resistance to LPS-induced lethality in CCR4(-/-) mice compared with wild-type mice. This study demonstrates that CCR4(-/-) mice are similarly resistant to challenge with other TLR agonists, as well as bacterial peritonitis. Resistance was associated with enhanced early leukocyte recruitment, increased TLR expression, a skewed type 2 cytokine/chemokine profile, and improved bacterial clearance. Macrophages from CCR4(-/-) mice exhibited many features consistent with alternative activation, including elevated secretion of type 2 cytokines/chemokines and the found in inflammatory zone 1 (FIZZ1) protein. MyD88-dependent NF-kappaB signaling was significantly down-regulated in CCR4(-/-) macrophages, whereas p38 MAPK and JNK activation were conversely increased. These data stress the importance of CCR4 in macrophage differentiation and innate immune responses to pathogens, as well as the involvement of chemokine receptor expression in TLR signaling regulation.     

Cardiovascular responses to nonrespiratory and respiratory arousals in a porcine model

Spontaneous and provoked nonrespiratoryarousals can be accompanied by a patterned hemodynamic response. Toinvestigate whether a patterned response is also elicited byrespiratory arousals, we compared nonrespiratory arousals (NRA) torespiratory arousals (RA) induced by airway occlusion during non-rapideye movement sleep. We monitored mean arterial blood pressure (MAP),heart rate, iliac and renal blood flow, and sleep stage in 7 pigsduring natural sleep. Iliac and renal vascular resistance werecalculated. Airway occlusions were obtained by manually inflating achronically implanted tracheal balloon during sleep. The balloon wasquickly deflated as soon as electroencephalogram arousal occurred. As previously reported, NRA generally elicited iliac vasodilation, renalvasoconstriction, little change in MAP, and tachycardia. In contrast,RA generally elicited iliac and renal vasoconstriction, an increase inMAP and tachycardia. The frequent occurrence of iliac vasoconstrictionand arterial pressure elevation following RA but not NRA suggests thatsleep state change alone does not account for the hemodynamic responseto airway occlusion during sleep.

     

Necator americanus and helminth co-infections: further down-modulation of hookworm-specific type 1 immune responses

Background

Helminth co-infection in humans is common in tropical regions of the world where transmission of soil-transmitted helminths such as Ascaris lumbricoides, Trichuris trichiura, and the hookworms Necator americanus and Ancylostoma duodenale as well as other helminths such as Schistosoma mansoni often occur simultaneously.

Methodology

We investigated whether co-infection with another helminth(s) altered the human immune response to crude antigen extracts from either different stages of N. americanus infection (infective third stage or adult) or different crude antigen extract preparations (adult somatic and adult excretory/secretory). Using these antigens, we compared the cellular and humoral immune responses of individuals mono-infected with hookworm (N. americanus) and individuals co-infected with hookworm and other helminth infections, namely co-infection with either A. lumbricoides, Schistosoma mansoni, or both. Immunological variables were compared between hookworm infection group (mono- versus co-infected) by bootstrap, and principal component analysis (PCA) was used as a data reduction method.

Conclusions

Contrary to several animal studies of helminth co-infection, we found that co-infected individuals had a further downmodulated Th1 cytokine response (e.g., reduced INF-γ), accompanied by a significant increase in the hookworm-specific humoral immune response (e.g. higher levels of IgE or IgG4 to crude antigen extracts) compared with mono- infected individuals. Neither of these changes was associated with a reduction of hookworm infection intensity in helminth co-infected individuals. From the standpoint of hookworm vaccine development, these results are relevant; i.e., the specific immune response to hookworm vaccine antigens might be altered by infection with another helminth.     

Activation and manipulation of host responses by a Gram-positive bacterium

The interaction between tomato plants and Clavibacter michiganensis subsp. michiganensis (Cmm) represents a model pathosystem to study the interplay between the virulence determinants of a Gram-positive bacterium and the attempt of a crop plant to counteract pathogen invasion. To investigate plant responses activated during this compatible interaction, we recently analyzed gene expression profiles of tomato stems infected with Cmm. This analysis revealed activation of basal defense responses that are typically observed upon plant perception of pathogen-associated molecular patterns. In addition, Cmm infection upregulated the expression of host genes related to ethylene synthesis and response. Further analysis of tomato plants impaired in ethylene perception and production demonstrated an important role for ethylene in the development of disease symptoms. Here we discuss possible molecular strategies used by the plant to recognize Cmm infection and possible mechanisms employed by the pathogen to interfere with the activation of plant defense responses and promote disease.Key words: tomato, Clavibacter michiganensis subsp. michiganensis, ethylene, basal defense, pathogen-associated molecular patternsLittle is known on the strategies employed by Gram-positive phytopathogenic bacteria to sense the presence of the host plant, penetrate and colonize tissue, and counteract plant defense responses. Also largely unexplored are the molecular mechanisms associated with detection of Gram-positive bacteria by the host plant and with the activation of attempted defense responses.Among the most devastating Gram-positive disease agents are actinobacteria of the genus Clavibacter whose subspecies cause systemic infections of the xylem in different plant species.¹ The subspecies Clavibacter michiganensis subsp. michiganensis (Cmm) causes bacterial wilt and canker of tomato (Solanum lycopersicum), an economically important disease causing yield losses worldwide.¹ In recent years important insight into the molecular mechanism of Cmm pathogenicity has been achieved,¹ and genome sequence of a Cmm strain has been established.² Major Cmm pathogenicity determinants are plasmid borne and include the β-1,4-endocellulase CelA,³ and the putative serine protease Pat-1.⁴ Additional genes important for virulence are located in a pathogenicity island of about 129 kb on the Cmm chromosome which has a relatively low G + C content and is required for effective Cmm colonization of tomato plants.²Tomato is an economically important crop amenable to genetic analysis and transformations. Many resources are available for this plant species, including germplasm collections, natural and induced mutants, an extensive expressed sequence tag database and an ongoing genome sequencing project.⁵ In addition, because of its experimental tractability, tomato plants have been widely used to study plant disease resistance and susceptibility. As genetic and molecular tools for both Cmm and tomato are in place, the tomato-Cmm pathosystem represents an excellent model to study the interplay between virulence determinants of a Gram-positive phytopathogenic bacterium and defense responses of a crop plant.To get insight into host responses occurring during the tomato-Cmm compatible interaction and molecular mechanisms associated with the development of wilt and canker disease symptoms, we recently analyzed gene expression profiles of tomato stems infected with Cmm.⁶ This analysis revealed a clear activation of basal defense responses, which are typically observed upon plant perception of pathogen-associated molecular patterns (PAMPs).⁷ These include production and scavenging of free oxygen radicals, induction of defense-related genes, enhanced protein turnover, and hormone biosynthesis. Interestingly, several tomato genes encoding proteins with characteristics of cell-surface receptors were differentially expressed in response to Cmm infection.⁶ These proteins can be considered as candidate receptors for Cmm PAMPs and include two receptor-like kinases, a homolog of the receptor for the fungal PAMP ethylene-inducing xylanase from Trichoderma viride,⁸ and the Ve1 resistance protein, which confers resistance in tomato to the vascular disease Verticillium wilt.⁹It remains to be elucidated what are the Cmm PAMPs perceived by tomato plants. Cold-shock protein from Gram-positive bacteria and different microbial patterns of Gram-negative bacteria, including lipopolysaccharides, flagellin, and the translational elongation factor EF-TU, were shown to act as PAMPs in plants.¹⁰ Similarly, Cmm cold shock protein or cell wall components, such as peptidoglycan, lipoteichoic acid, and lipopeptides, which function as Gram positive-derived PAMPs in animal systems¹¹, may act as PAMPs during the tomato-Cmm interaction. Additional possible Cmm PAMPs are exopolysaccharides, which are produced in large amounts by the bacterium and may interact directly with surface-exposed plant proteins.¹ The numerous extracellular cell wall degrading enzymes secreted by Cmm may also function as PAMPs, as observed for the fungal ethylene-inducing xylanase.^2,12 Alternatively, by virtue of their hydrolytic activity, these enzymes may release plant cell wall fragments that are recognized by PAMP receptors. Indeed, different β-glucan fragments released from plant cell walls were shown to elicit plant basal defense responses.^13,14How Cmm copes with the activation of basal defense responses is largely unknown. Many potential virulence determinants that might interfere with the plant defense reaction are clustered in the Cmm pathogenicity island, which is essential for effective plant colonization.² Several extracellular serine proteases are encoded in this region and inactivation of part of them by gene replacement drastically reduced Cmm colonization of tomato plants.² Although their targets are still unknown, these proteins might interfere with plant signaling pathways as it was described for certain cysteine proteases that serves in Gram-negative bacteria as suppressors of plant defenses.¹⁵ An additional candidate for interference with plant signaling may be a tomatinase, also encoded in the Cmm pathogenicity island, because hydrolysis products of α-tomatine were shown to suppress plant defense responses in a fungal system.¹⁶In addition to detecting the activation of basal defense responses, host gene expression profiling during the tomato-Cmm interaction unraveled the involvement of ethylene in disease development.⁶ In fact, Cmm infection of tomato stems was found to induce expression of host genes related to ethylene biosynthesis and response (Fig. 1).⁶ Further analysis of ethylene-insensitive Never ripe mutants and transgenic plants with reduced ethylene synthesis indicated that ethylene is required for normal development of wilting symptoms (Fig. 2), but not for the activation of defense-related genes or bacterial colonization.⁶ We hypothesize that during infection ethylene synthesis and response are manipulated by Cmm virulence determinants to promote disease. Alternatively, ethylene is released as part of the host responses activated by bacterial recognition, or as a result of tissue maceration. In line with our first hypothesis, the type III effectors AvrPto and AvrPtoB from Pseudomonas syringae pv. tomato were shown to promote enhanced disease symptoms in tomato leaves, in part, by upregulating genes involved in ethylene production.¹⁷ Interestingly, expression in tomato plants of AvrPto or AvrPtoB, and infection with Cmm resulted in the upregulation of the SlACO1 gene encoding the key enzyme of ethylene biosynthesis ACC oxidase.^6,17Open in a separate windowFigure 1Kinetics of ACC oxidase (ACO) gene expression in tomato plants inoculated with Cmm. Six-week-old tomato plants were infected with a Cmm suspension (10⁸ cfu/ml) or mock-inoculated. Total RNA was extracted from stem samples harvested at the indicated day post-inoculation (dpi) and subjected to Northern blot analysis using as probe a 550 bp fragment of the SlACO1 gene, which shares high homology with other ACO family members (upper). Ethidium bromide staining shows the amount of RNA loaded in each lane (lower).Open in a separate windowFigure 2Effect of impaired ethylene sensitivity on development of wilt symptoms in tomato plants infected with Cmm. Six-week-old plants were infected with a Cmm suspension (10⁸ cfu/ml) and examined for development of wilt symptoms during a 20-day period. The percentage of plants showing wilt symptoms was calculated in a group of at least 30 plants for the ethylene-insensitive mutant Never ripe and wild-type Pearson plants. Data are representative of two independent experiments.In conclusion, future research challenges for understanding how host responses are regulated by the plant and manipulated by a Gram-positive bacterium will be the isolation of Cmm PAMPs and their plant receptors, the identification of Cmm virulence determinants and the elucidation of their mode of action.     

Network theory reveals principles of spliceosome structure and dynamics

1. Download : Download high-res image (283KB)
2. Download : Download full-size image

     

Multicellular spatial model of RNA virus replication and interferon responses reveals factors controlling plaque growth dynamics

Respiratory viruses present major public health challenges, as evidenced by the 1918 Spanish Flu, the 1957 H2N2, 1968 H3N2, and 2009 H1N1 influenza pandemics, and the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. Severe RNA virus respiratory infections often correlate with high viral load and excessive inflammation. Understanding the dynamics of the innate immune response and its manifestations at the cell and tissue levels is vital to understanding the mechanisms of immunopathology and to developing strain-independent treatments. Here, we present a novel spatialized multicellular computational model of RNA virus infection and the type-I interferon-mediated antiviral response that it induces within lung epithelial cells. The model is built using the CompuCell3D multicellular simulation environment and is parameterized using data from influenza virus-infected cell cultures. Consistent with experimental observations, it exhibits either linear radial growth of viral plaques or arrested plaque growth depending on the local concentration of type I interferons. The model suggests that modifying the activity of signaling molecules in the JAK/STAT pathway or altering the ratio of the diffusion lengths of interferon and virus in the cell culture could lead to plaque growth arrest. The dependence of plaque growth arrest on diffusion lengths highlights the importance of developing validated spatial models of cytokine signaling and the need for in vitro measurement of these diffusion coefficients. Sensitivity analyses under conditions leading to continuous or arrested plaque growth found that plaque growth is more sensitive to variations of most parameters and more likely to have identifiable model parameters when conditions lead to plaque arrest. This result suggests that cytokine assay measurements may be most informative under conditions leading to arrested plaque growth. The model is easy to extend to include SARS-CoV-2-specific mechanisms or to use as a component in models linking epithelial cell signaling to systemic immune models.     

Species-specific treatment effects of helminth/HIV-1 co-infection: a systematic review and meta-analysis

In sub-Saharan Africa, over 22 million people are estimated to be co-infected with both helminths and HIV-1. Several studies have suggested that de-worming individuals with HIV-1 may delay HIV-1 disease progression, and that the benefit of de-worming may vary by individual helminth species. We conducted a systematic review and meta-analysis of the published literature to determine the effect of treatment of individual helminth infections on markers of HIV-1 progression (CD4 count and HIV viral load). There was a trend towards an association between treatment for Schistosoma mansoni and a decrease in HIV viral load (Weighted mean difference (WMD)=-0·10; 95% Confidence interval (CI): -0·24, 0·03), although this association was not seen for Ascaris lumbricoides, hookworm or Trichuris trichiura. Treatment of A. lumbricoides, S. mansoni, hookworm or T. trichiura was not associated with a change in CD4 count. While pooled data from randomized trials suggested clinical benefit of de-worming for individual helminth species, these effects decreased when observational data were included in the pooled analysis. While further trials are needed to confirm the role of anthelmintic treatment in HIV-1 co-infected individuals, providing anthelmintics to individuals with HIV-1 may be a safe, inexpensive and practical intervention to slow progression of HIV-1.     

Helicobacter pylori and Schistosoma japonicum co-infection in a Chinese population: helminth infection alters humoral responses to H. pylori and serum pepsinogen I/II ratio

The effects of helminth infection on humoral IgG responses and clinical outcome of gastric Helicobacter pylori infection are unknown. IgG and IgG subclass responses to H. pylori and serum pepsinogen I/II ratio, a marker of gastric atrophy, were investigated in a Schistosoma japonicum prevalent Chinese population. H. pylori, CagA and IgG subclass responses were assayed by ELISA. Serum pepsinogen I and pepsinogen II were assayed by ELISA and the pepsinogen I/II ratio determined. In 150 subjects, infection with S. japonicum and H. pylori was 55.3% and 51.3%, respectively. H. pylori IgG titres and CagA seropositivity were significantly lower (P<0.05) in co-infected subjects, and differences in H. pylori IgG isotype responses were evident. In H. pylori positives, a significantly higher (P<0.05) pepsinogen I/II ratio was observed in co-infected subjects. The difference between S. japonicum positive and negative subjects was only evident in H. pylori CagA seronegative subjects. In conclusion, S. japonicum co-infection with H. pylori is associated with alterations in IgG responses to H. pylori and less gastric atrophy.     

Bacterial-epithelial contact is a key determinant of host innate immune responses to enteropathogenic and enteroaggregative Escherichia coli

Background

Enteropathogenic (EPEC) and Enteroaggregative (EAEC) E. coli have similar, but distinct clinical symptoms and modes of pathogenesis. Nevertheless when they infect the gastrointestinal tract, it is thought that their flagellin causes IL-8 release leading to neutrophil recruitment and gastroenteritis. However, this may not be the whole story as the effect of bacterial adherence to IEC innate response(s) remains unclear. Therefore, we have characterized which bacterial motifs contribute to the innate epithelial response to EPEC and EAEC, using a range of EPEC and EAEC isogenic mutant strains.

Methodology

Caco-2 and HEp-2 cell lines were exposed to prototypical EPEC strain E2348/69 or EAEC strain O42, in addition to a range of isogenic mutant strains. E69 [LPS, non-motile, non-adherent, type three secretion system (TTSS) negative, signalling negative] or O42 [non-motile, non-adherent]. IL-8 and CCL20 protein secretion was measured. Bacterial surface structures were assessed by negative staining Transmission Electron Microscopy. The Fluorescent-actin staining test was carried out to determine bacterial adherence.

Results

Previous studies have reported a balance between the host pro-inflammatory response and microbial suppression of this response. In our system an overall balance towards the host pro-inflammatory response is seen with the E69 WT and to a greater extent O42 WT, which is in fit with clinical symptoms. On removal of the external EPEC structures flagella, LPS, BFP, EspA and EspC; and EAEC flagella and AAF, the host inflammatory response is reduced. However, removal of E69 lymphostatin increases the host inflammatory response suggesting involvement in the bacterial mediated anti-inflammatory response.

Conclusion

Epithelial responses were due to combinations of bacterial agonists, with host-bacterial contact a key determinant of these innate responses. Host epithelial recognition was offset by the microbe''s ability to down-regulate the inflammatory response. Understanding the complexity of this host-microbial balance will contribute to improved vaccine design for infectious gastroenteritis.     

Innate and adaptive immune responses to an intracellular bacterium,Francisella tularensis live vaccine strain

The immune response to intracellular bacterium, Francisella tularensis, which causes tularemia and is proposed to be a potential bioterrorism pathogen, has been studied in mice using the attenuated live vaccine strain (LVS). Here we review this infection model, which provides a convenient means of studying protective immune mechanisms not only for Francisella, but also for the large and important class of intracellular pathogens.     

Innate and adaptive immune responses to nonvascular xenografts: evidence that macrophages are direct effectors of xenograft rejection

Nonvascularized xenograft rejection is T cell mediated, but is dependent on initial macrophage (Mphi) infiltration. We developed an i.p. transplant model to define the roles of Mphi and T cells in xenograft rejection. Nonobese diabetic or BALB/c mice were injected i.p. with xenogeneic, allogeneic, or syngeneic cells, and the responding cells in subsequent lavages were assessed by flow cytometry and adoptive transfer. Neutrophils and monocytes/elicited Mphi were rapidly recruited in response to xenogeneic pig (PK15 or spleen) cells and, to a significantly lesser extent, allogeneic cells. These innate responses preceded T cell infiltration and occurred in their absence in SCID mice. Syngeneic cells induced negligible neutrophil or Mphi responses. Neutrophils and Mphi induced by xenogeneic cells in SCID mice stimulated T cell recruitment after transfer to immunocompetent mice. T cells in turn were required for Mphi activation and xenogeneic cell rejection. Thus, Mphi harvested from immunocompetent but not SCID mice injected with xenogeneic cells expressed activation markers and rejected xenogeneic cells when transferred into SCID mice. These findings demonstrate the interdependent roles of Mphi and T cells in xenograft rejection. The requirement for Mphi reflects their ability to mount a rapid, local innate response that stimulates T cell recruitment and, having received T cell help, to act as direct effectors of rejection.     

Time delay as a key factor of model plankton dynamics

Studies of the mechanisms underlying complex dynamics of ecological systems at various spatial and time scales bring increasing awareness that complexity is an intrinsic feature of ecological functioning. This paper is to investigate the role of such an ecologically significant parameter as the time delay due to maturation processes in the complex plankton dynamics. We show that the time lag T1, associated with the zooplankton maturation period can lead to essential changes in the plankton dynamics. Particularly, we show that the coexistence of limit cycle and chaotic attractor we have recently found to be typical of the system at T1 = 0 [A.B. Medvinsky, I.A. Tikhonova, R.R. Aliev, B.-L. Li, Z.-S. Lin, H. Malchow, Patchy environment as a factor of complex plankton dynamics, Phys. Rev. E 64 (2001) 021915] is replaced by pure chaotic plankton dynamics as T1 becomes more than a critical value. The results obtained imply that chaos is a rather common phenomenon in the plankton functioning.     

Arabidopsis thaliana model system reveals a continuum of responses to root endophyte colonization

We surveyed the non-mycorrhizal model plant Arabidopsis thaliana microscopically for its ability to form dark septate endophyte (DSE) symbioses in field, greenhouse, and laboratory studies. The laboratory studies were also used to estimate host growth responses to 34 Periconia macrospinosa and four Microdochium sp. isolates. Consistent with broad host range observed in previous experiments, field-, greenhouse-, and laboratory-grown A. thaliana were colonized by melanized inter- and intracellular hyphae and microsclerotia or chlamydospores indicative of DSE symbiosis. Host responses to colonization were variable and depended on the host ecotype. On average, two A. thaliana accessions (Col-0 and Cvi-0) responded negatively, whereas one (Kin-1) was unresponsive, a conclusion consistent with our previous analyses with forbs native to the field site where the fungi originate. Despite the average negative responses, examples of positive responses were also observed, a conclusion also congruent with earlier studies. Our results suggest that A. thaliana has potential as a model for more detailed dissection of the DSE symbiosis. Furthermore, our data suggest that host responses are controlled by variability in the host and endophyte genotypes.     

A joint individual‐based model coupling growth and mortality reveals that tree vigor is a key component of tropical forest dynamics

Tree vigor is often used as a covariate when tree mortality is predicted from tree growth in tropical forest dynamic models, but it is rarely explicitly accounted for in a coherent modeling framework. We quantify tree vigor at the individual tree level, based on the difference between expected and observed growth. The available methods to join nonlinear tree growth and mortality processes are not commonly used by forest ecologists so that we develop an inference methodology based on an MCMC approach, allowing us to sample the parameters of the growth and mortality model according to their posterior distribution using the joint model likelihood. We apply our framework to a set of data on the 20‐year dynamics of a forest in Paracou, French Guiana, taking advantage of functional trait‐based growth and mortality models already developed independently. Our results showed that growth and mortality are intimately linked and that the vigor estimator is an essential predictor of mortality, highlighting that trees growing more than expected have a far lower probability of dying. Our joint model methodology is sufficiently generic to be used to join two longitudinal and punctual linked processes and thus may be applied to a wide range of growth and mortality models. In the context of global changes, such joint models are urgently needed in tropical forests to analyze, and then predict, the effects of the ongoing changes on the tree dynamics in hyperdiverse tropical forests.