Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851341 (infestation)
 10,121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical signs of a Sarcoptes scabiei (De Geer) (Acari: Sarcoptidae) infestation are initially delayed, which suggests that the mites can depress the immune/inflammatory response. The purpose of this study was to investigate the modulatory properties of scabies mites in vivo at the gene expression level in a secondary lymphoid organ that is involved in initiating an immune response to the parasite. We found that substances from scabies mites influenced the expression of mRNA for molecules that participate in the sequestering of lymphocytes in the periarteriolar lymphoid sheath, primary follicle, and marginal zone of the spleen. Mice exposed to live scabies mites exhibited decreased mRNA expression for the adhesion molecules intercellular adhesion molecule (ICAM)-1, ICAM-2 and L-selectin; the cytokines tumor necrosis factor (TNF)alpha and CCL5; and the receptors for several other cytokines including TNF and interferon gamma. In addition, exposure to live mites or vaccination with a scabies extract resulted in reduced expression of mRNA for B7-2, CD40, CD4, CD8, and CD45, thereby potentially reducing the physical interactions between B cells and T-helper (Th)2 helper cells, between Th1 and Tc cells, and between T-helper cells and antigen-presenting cells, thus depressing their function in response to thymus-dependent antigen. Live scabies mites also depressed expression of toll-like receptors 2, 4, and 6. In conclusion, our results indicate that live mites produce substances that can down-regulate expression of adhesion molecules, cytokines, chemokines, chemokine receptors, and lymphocyte surface molecules involved in leukocyte sequestering and the interaction of B and T cells during activation of an immune response in the spleen.
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PMID:In vivo evidence that Sarcoptes scabiei (Acari: Sarcoptidae) is the source of molecules that modulate splenic gene expression. 1804 6

Helminth parasites drive dominant Th2 responses through an as yet unidentified pathway. We have previously shown that the rodent gastrointestinal nematode Nippostrongylus brasiliensis secretes products which selectively activate in vitro-derived dendritic cells to induce Th2 responses on in vivo transfer. We now show that, during active infection with this parasite, the draining mesenteric lymph node dendritic cell population is altered significantly. Although there is substantial expansion of DC numbers during infection, the CD86(hi)-CD8alpha(int)-CD11b(-) subset is markedly diminished, and expression levels of CD40, CD86 and CD103 are reduced. Notably, the reduced frequency of CD8alpha(int) DCs is evident only in those mesenteric lymph nodes draining the anterior site of infestation. In infections with the longer lived Heligmosomoides polygyrus, the proportion of CD8alpha(int) DCs in the MLNC falls to below 10% of total DC numbers by 35 days post-infection. Further, infection alters TLR responsiveness, as IL-12 production (as measured by ex vivo intracellular staining of CD11c(+) DCs) in response to LPS stimulation is reduced, while IL-6, TNF-alpha and in particular, IL-10 all increase following infection with either nematode parasite. These changes suggest the possibility that helminth parasites modulate gastrointestinal immunity both by inhibiting migration of CD8alpha(int) DCs to the draining lymph nodes, and modifying DC responsiveness in a manner which favours a Th2 outcome.
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PMID:Dynamics of CD11c(+) dendritic cell subsets in lymph nodes draining the site of intestinal nematode infection. 1976 74