Hymenolepis diminuta: Effect of infection on ion transport in colon and blood picture of rats

The aim of this study was to examine the effect of an infection with Hymenolepis diminuta on ion transport in an isolated colon and blood picture of rats. Fifty rats were orally infected with five cysticercoids of H. diminuta. The experimental groups of rats were assigned to four groups: group I - 8 days post-infection (dpi), group II - 16 dpi, group III - 40 dpi and group IV- 60 dpi. The control group comprised non-infected rats. The experiments consisted of measuring the transepithelial electrical potential difference (PD) and the transepithelial electrical resistance (R) of the rat colon under controlled conditions as well as during mechanical stimulation (MS) using a modified Ussing chamber. Ion transport was modified using inhibitors of the epithelial sodium channel (amiloride - AMI) and the epithelial chloride channel (bumetanide - BUME), and also using capsaicin (CAPSA), a substance which activates C-fibres. The experimental data presented in this study indicates that experimental hymenolepidosis inhibits sodium and chloride ion transport in the epithelium of the rat colon, with preserved tight junction continuity (except at 40 dpi) and a decreased mechanical sensitivity. The effect of capsaicin on ion transport in the rat colon was varied. In control rats it increased ionic current, and in H. diminuta-infected rats it did not cause any changes in PD.Blood picture in this study showed a statistically significantly lower red blood cells (RBC) count and haemoglobin (HGB) concentration in infected rats in comparison to non-infected. Red cell distribution width (RDW) values and platelet (PLT) count were negatively correlated with the duration of infection, whereas mean corpuscular volume (MCV) value was positively correlated. We did not observe leukocytosis during infection, and amongst the differential leukocyte counts eosinophils and basophils showed statistically significant lower values in infected rats in comparison to non-infected.Our results indicate that hymenolepidosis is associated with the activation of inflammatory mediators and stimulation of nervous fibres, which significantly affects the function of ion channels in the epithelium of the colon in the host. At the same time, a significant decrease in eosinophil count during infection suggests that such an infection did not trigger a strong immunological reaction in rats.     

Activation of B cells by non-canonical helper signals

Cognate interaction between T and B lymphocytes of the adaptive immune system is essential for the production of high-affinity antibodies against microbes, and for the establishment of long-term immunological memory. Growing evidence shows that-in addition to presenting antigens to T and B cells-macrophages, dendritic cells and other cells of the innate immune system provide activating signals to B cells, as well as survival signals to antibody-secreting plasma cells. Here, we discuss how these innate immune cells contribute to the induction of highly diversified and temporally sustained antibody responses, both systemically and at mucosal sites of antigen entry.     

Tick resistance: basophils in skin reactions of resistant guinea pigs

Guinea pigs acquired resistance to Dermacentor andersoni larvae. Administration of the immunosuppressant, Methotrexate, prevented the acquisition of resistance. Resistant hosts allowed relatively very few larvae to engorge, and showed marked infiltration of the infested skin by basophil leucocytes. Particular high concentrations of basophils occurred in vesicles in the hyperplastic epidermis beneath the mouth-parts of attached larvae. These changes appear similar to Cutaneous Basophil Hypersensitivity reactions.     

The connective connection: interstitial cells of Cajal (ICC) and ICC-like cells establish synapses with immunoreactive cells. Electron microscope study in situ

We present transmission electron microscope (TEM) evidence that ICC and ICC-like cells frequently establish close contacts (synapses) with several types of immunoreactive cells (IRC): lymphocytes, plasma cells, eosinophils, basophils, macrophages and mast cells. Such synapses were found in various organs: human mammary gland and myometrium, as well as rat stomach, gut, bladder and uterus. Specimens were observed by conventional TEM on ultrathin sections. Based on morphometric analyses and computer-aided 3-D reconstructions from serial sections, we propose an operational definition of ICC-IRC synapses: cell-to-cell close contacts where the two cells are separated by only approximately 15 nm, equivalent to twice the plasmalemmal thickness. Two types of such synapses were found: (i) uniform ('plain') synapses (PS). close contact extending for >200 nm, and (ii) multi-contact ('kiss and run') synapses (MS)--with multiple, focal, close-contact points alternating with regions of wider intermembrane distance. For instance, a typical PS between a rat bladder ICC-like cell and an eosinophil was 2.48 microm long and 11+/-4 nm wide. By contrast, a MS synapse in rat myometrium (between an ICC-like cell and an eosinophil) was 8.64 microm long and had 13 contact points. The synaptic cleft measured 15+/-8 nm at contact points and approximately 100 nm or more in wider areas. These synapses are different from gap junctions usually seen between ICC and between ICC and smooth muscle cells. We previously proposed that ICC-like cells might represent stromal progenitor cells, participate in juxtacrine/paracrine signaling and play a role in immune surveillance. The nanoscopic distances between the two contiguous membranes suggest a juxtacrine cell-to-cell signaling (chemical synapse), via juxtacrinins, a specific case of phenomenins. However, the (micro)vesicles found in the synaptic cleft may correspond to an exosome-based mechanism.     

A Mysterious Malady: the Malachowski-Wright-Giemsa Stain to the Rescue

Abstract

A patient entered hospital with a puzzling absolute monocytosis. Admitting blood smears had been stained with Diff-Quik, a Romanowsky stain. When additional smears were stained using a standard Malachowski-Wright-Giemsa method, the reason for the monocytosis became abundantly clear.     

Multiorgan autoimmunity in a Turner syndrome patient with partial monosomy 2q and trisomy 10p

Turner syndrome is a condition caused by numeric and structural abnormalities of the X chromosome, and is characterized by a series of clinical features, the most common being short stature and gonadal dysgenesis. An increased frequency of autoimmune diseases as well as an elevated incidence of autoantibodies has been observed in Turner patients.     

Cutaneous and systemic cellular responses induced by the feeding of the argasid tick Ornithodoros parkeri

Carolyn M. Johnston and Stephen J. Brown 1985. Cutaneous and systemic cellular responses induced by the feeding of the argasid tick Ornithodoros parkeri. International Journal for Parasitology15: 621–628. Initial feeding by Ornithodoros parkeri ticks induced a significant blood basophilia in guinea pigs, with a minimal cutaneous basophil response. Hosts challenged 14 days later, however, exhibited significantly depressed blood basophil levels associated with a marked accumulation of these cells at tick feeding sites in the tissue. Blood eosinophil levels in primary and secondary hosts were comparable, but eosinophil levels at tick feeding sites in challenged animals were significantly greater than levels in primary hosts. Furthermore, challenge tick feeding resulted in the activation of primary tick feeding sites on the opposite flank that became erythematous 90 min after challenge and indurated within 24 h. Histologically, these activated primary feeding sites 90 min after challenge on the opposite flank were marked by a dominant eosinophil response (314 ± 128 cells, 59% of the infiltrate) with a marked basophil component (145 ± 67 cells, 28% of the infiltrate) that resembled the active challenge feeding sites 24 h after infestation (24 ± 52 cells, 76% of the infiltrate); 90 min after challenge active feeding sites had a weak basophil response (2 ± 1 cells) similar to uninfested controls. These results suggest the chronic nature of tick bites with an apparent continual recruitment of basophils that is probably a result of slow antigen release over time by appropriately sensitized antigen presenting cells. Primary tick feeding sites in guinea pigs previously exposed to Xenopsylla cheopis fleas, on the opposite flank, contained a marked eosinophilia (63 ± 25 cells) compared to primary tick feeding sites in naive guinea pigs (2 ± 0 cells); suggesting the possibility of cross reactivity between flea and tick antigens     

MD-2 is required for the full responsiveness of mast cells to LPS but not to PGN

To address the role played by MD-2 in mast cell recognition of LPS, we examined bone marrow-derived mast cells (BMMCs) from MD-2 gene-targeted mice. BMMCs from MD-2-/- mice showed impaired cytokine production (TNF-alpha, IL-6, IL-13, and IL-1beta) in response to LPS from Escherichia coli, but not to peptidoglycan (PGN) from Staphylococcus aureus. In a mast cell-dependent acute septic model, MD-2 deficiency of mast cell resulted in significantly higher mortality due to defective neutrophil recruitment and the production of cytokines in the peritoneal cavity, which was similar to mice with TLR4-deficient mast cells. The TLR2-dependent activation of skin mast cells by PGN was not altered by the absence of MD-2 in vivo. Collectively, MD-2 is essential for the recognition of LPS by TLR4 but not for that of PGN by TLR2 of mast cells.