02096nas a2200361   4500000000100000008004100001653001200042653001300054653002000067653002100087653001100108653002000119653003100139653002800170653000900198653003100207653000900238653002400247653001800271653001700289653003400306653001800340653002400358653003200382100001400414700001300428700001200441245015900453300001100612490000700623520109000630022001401720       2012                            d10aAnimals10aArginine10aCells, Cultured10aCyclooxygenase 210aFemale10aGene Expression10aGene Expression Regulation10aMacrophages, Peritoneal10aMale10aMatrix Metalloproteinase 910aMice10aMice, Inbred BALB C10aMycobacterium10aNitric Oxide10aNitric Oxide Synthase Type II10aRNA Transport10aSignal Transduction10aTumor Necrosis Factor-alpha1 aPandey RK1 aDahiya Y1 aSodhi A00aMycobacterium indicus pranii downregulates MMP-9 and iNOS through COX-2 dependent and TNF-α independent pathway in mouse peritoneal macrophages in vitro.  a348-560 v143 a<p>Despite the popular belief that granulomas are innate immune mechanism to restrict mycobacterial growth, evidences suggest that granulomas facilitate growth of Mycobacterium by recruiting large numbers of uninfected macrophages to the site of infection. Matrix metalloproteinase-9 (MMP-9) has been shown to be directly involved in recruitment of macrophages at the site of infection, contributing to nascent granuloma maturation and bacterial growth. In this manuscript it is reported that heat-killed Mycobacterium indicus pranii (MIP) leads to a significant downregulation of MMP-9 in murine peritoneal macrophages in vitro. The downregulation of MMP-9 is mediated through cyclooxygenase-2 (COX-2), but independent of tumor necrosis factor-α (TNF-α). By limiting nuclear to cytoplasmic export of COX-2 and iNOS transcripts, MIP inhibits excessively-high levels of nitric oxide which can be damaging to the host during acute phases of infection. MIP has been shown to provide clinical improvement in all phases of leprosy and used for treatment of leprosy and tuberculosis.</p>
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