A novel adherence assay for Bordetella pertussis using tracheal organ cultures

Abstract In a novel adherence model using tracheal rings removed from Papio anubis , we have demonstrated a functional role for the fimbriae of Bordetella pertussis . When compared to wild-type strains, B. pertussis mutants specifically deficient in fimbriae adhered less well to the tracheal rings but better to Vero (Green monkey kidney) cells. In contrast, mutants deficient in filamentous haemagglutinin (FHA) production had reduced adherence to both Vero cells and the tracheal rings. These observations indicate that the fimbriae of B. pertussis , like those of many other bacterial pathogens, may play an important role in the initial stages of colonisation.     

Antitussive activity of the fruit extract of Emblica officinalis Gaertn. (Euphorbiaceae)

The antitussive activity of Emblica officinalis Gaertn. (E. officinalis, Fam. Euphorbiaceae) was tested in conscious cats by mechanical stimulation of the laryngopharyngeal and tracheobronchial mucous areas of airways. The results showed that at a dose of 50 mg/kg body wt. perorally, the cough suppressive effect of E. officinalis is not unambiguous. A higher dose (200 mg/kg body wt.) of this substance perorally was more effective, especially in decreasing the number of cough efforts (NE), frequency of cough (NE/min(-1)) and the intensity of cough attacks in inspirium (IA+) and expirium (IA-) was more pronounced. These results showed that the cough suppressive activity of E. officinalis is dose-dependent. We could also demonstrate that the antitussive activity of E. officinalis is less effective than shown by the classical narcotic antitussive drug codeine, but more effective than the non-narcotic antitussive agent dropropizine. It is supposed that the antitussive activity of the dry extract of Emblica officinalis is due not only to antiphlogistic, antispasmolytic and antioxidant efficacy effects, but also to its effect on mucus secretion in the airways.     

Can we learn from the pathogenetic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae?

The purpose of this review-hypothesis is to discuss the literature which had proposed the concept that the mechanisms by which infectious and inflammatory processes induce cell and tissue injury, in vivo, might paradoxically involve a deleterious synergistic 'cross-talk', among microbial- and host-derived pro-inflammatory agonists. This argument is based on studies of the mechanisms of tissue damage caused by catalase-negative group A hemolytic streptococci and also on a large body of evidence describing synergistic interactions among a multiplicity of agonists leading to cell and tissue damage in inflammatory and infectious processes. A very rapid cell damage (necrosis), accompanied by the release of large amounts of arachidonic acid and metabolites, could be induced when subtoxic amounts of oxidants (superoxide, oxidants generated by xanthine-xanthine oxidase, HOCl, NO), synergized with subtoxic amounts of a large series of membrane-perforating agents (streptococcal and other bacterial-derived hemolysins, phospholipases A2 and C, lysophosphatides, cationic proteins, fatty acids, xenobiotics, the attack complex of complement and certain cytokines). Subtoxic amounts of proteinases (elastase, cathepsin G, plasmin, trypsin) very dramatically further enhanced cell damage induced by combinations between oxidants and the membrane perforators. Thus, irrespective of the source of agonists, whether derived from microorganisms or from the hosts, a triad comprised of an oxidant, a membrane perforator, and a proteinase constitutes a potent cytolytic cocktail the activity of which may be further enhanced by certain cytokines. The role played by non-biodegradable microbial cell wall components (lipopolysaccharide, lipoteichoic acid, peptidoglycan) released following polycation- and antibiotic-induced bacteriolysis in the activation of macrophages to release oxidants, cytolytic cytokines and NO is also discussed in relation to the pathophysiology of granulomatous inflammation and sepsis. The recent failures to prevent septic shock by the administration of only single antagonists is disconcerting. It suggests, however, that since tissue damage in post-infectious syndromes is caused by synergistic interactions among a multiplicity of agents, only cocktails of appropriate antagonists, if administered at the early phase of infection and to patients at high risk, might prevent the development of post-infectious syndromes.