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Immunological Control (immunological + control)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Interferon-,-mediated activation of enterocytes in immunological control of Encephalitozoon intestinalis infection

PARASITE IMMUNOLOGY, Issue 1 2009
N. CHOUDHRY
SUMMARY The microsporidian Encephalitozoon intestinalis develops within intestinal epithelial cells (enterocytes) and is an important opportunistic diarrhoeal pathogen associated with AIDS. Little is known about the protective immune response against the parasite although in mice IFN-, is involved and is required to prevent dissemination of the infection to other organs. The present study was designed to establish a suitable short-term in vitro culture technique for E. intestinalis that would enable studies of the role of cytokines such as IFN-, in the effector phase of immunity. Encephalitozoon intestinalis reproduced considerably better in the murine enterocyte cell line CMT-93 than in the three human enterocyte cell lines Caco-2, HT29 and HCT-8. Treatment of CMT-93 cells with IFN-, significantly reduced parasite reproduction in a dose- and time-dependent manner. IFN-, also inhibited development of the parasite in Caco-2 cells. Neither production of NO nor Fe deprivation appeared to be involved in IFN-,-mediated parasite killing. However studies suggested that tryptophan catabolism by indoleamine 2,3-dioxygenase played an important part in inactivation of E. intestinalis. [source]

Immune-mediated alteration in gut physiology and its role in host defence in nematode infection

PARASITE IMMUNOLOGY, Issue 8-9 2004
W. I. Khan
SUMMARY Activation of the mucosal immune system of the gastrointestinal tract in nematode infection results in altered intestinal physiology, which includes changes in intestinal motility and mucus production. These changes are considered to be under direct immunological control rather than a non-specific consequence of the inflammatory reaction to the infective agent. However, little is known about the immunological basis for the changes in intestinal physiology accompanying nematode infection, or the precise role of these changes in host defence, which remains an important area to explore. In this review we describe the mechanisms by which the immune response to nematode infection influences the changes in two major cells of intestinal physiology, namely smooth muscle and goblet cells, and how these changes in intestinal physiology contribute to the host defence. Data clearly demonstrate that the T helper (Th) 2 type immune response generated by nematode infection plays an important role in the development of infection-induced intestinal muscle hypercontractility and goblet cell hyperplasia and that these immune-mediated changes in intestinal physiology are associated with worm expulsion. These observations strongly suggest that intestinal muscle contractility, goblet cell hyperplasia and worm expulsion share a common immunological basis and may be causally related. These data not only provide insights into host defence in nematode infection in the context of muscle function and goblet cell response, but also have broad implications in elucidating the pathophysiology of a wide range of gastrointestinal disorders associated with altered gut physiology. [source]

Host cell-mediated responses to infection with Cryptosporidium

PARASITE IMMUNOLOGY, Issue 12 2000
V. McDonald
The coccidian Cryptosporidium infects epithelial cells of a variety of vertebrate hosts and is the causative agent of cryptosporidiosis. In mammals, including humans and domestic animals, C. parvum infects the gastrointestinal tract producing an acute watery diarrhoea and weight loss. CD4+ T-cell-deficient hosts have increased susceptibility to infection with the parasite and may develop severe life-threatening complications. The host responses which induce protective immunity and contribute to pathogenesis are poorly understood. In the immunological control of infection, recent studies with murine infection models suggest that IFN-, plays a key role in a partially protective innate immunity against infection identified in immunocompromised mice and also in the elimination of infection mediated by CD4+ T-cells. At the mucosal level, CD4+ intraepithelial lymphocytes are involved in the control of cryptosporidial infection, acting at least in part through production of IFN-, which has a direct inhibitory effect on parasite development in enterocytes. Primary infection of ruminants induces an intestinal inflammatory response in which increased numbers of various T-cell subpopulations appear in the villi. In addition, infection results in increased intestinal expression of pro-inflammatory cytokines such as IL-12, IFN-, and TNF-,. Because these cytokines appear to be important in the aetiology of inflammatory bowel disease, it is possible that they are involved in the mucosal pathogenesis of cryptosporidiosis. [source]

Gut motor function: immunological control in enteric infection and inflammation

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2006
W. I. Khan
Summary Alteration in gastrointestinal (GI) motility occurs in a variety of clinical settings which include acute enteritis, inflammatory bowel disease, intestinal pseudo-obstruction and irritable bowel syndrome (IBS). Most disorders affecting the GI tract arise as a result of noxious stimulation from the lumen via either microbes or chemicals. However, it is not clear how injurious processes initiated in the mucosa alter function in the deeper motor apparatus of the gut wall. Activation of immune cells may lead to changes in motor-sensory function in the gut resulting in the development of an efficient defence force which assists in the eviction of the noxious agent from the intestinal lumen. This review addresses the interface between immune and motor system in the context of host resistance based on the studies in murine model of enteric nematode parasite infection. These studies clearly demonstrate that the infection-induced T helper 2 type immune response is critical in producing the alterations of infection-induced intestinal muscle function in this infection and that this immune-mediated alteration in muscle function is associated with host defence mechanisms. In addition, by manipulating the host immune response, it is possible to modulate the accompanying muscle function, and this may have clinical relevance. These observations not only provide valuable information on the immunological control of gut motor function and its role in host defence in enteric infection, but also provide a basis for understanding pathophysiology of gastrointestinal motility disorders such as in IBS. [source]