Mycobacterium avium subsp. paratuberculosis (M. ptb) is the causative agent of Johne’s disease, a chronic granulomatous enteritis in ruminants, characterized by thickening of the intestinal wall and progressive wasting leading to death of the animal. Current estimates indicate that Johne’s disease is one of the most costly infectious diseases of livestock in many countries including Iran. The immune response to mycobacterial infection involves phagocytosis of organisms by mononuclear phagocytes and sequestration within phagosomes. The capacity of the organism to prevent macrophage activation and phagosome maturation and to attenuate induction of a Th1 immune response appears to largely determine its pathogenicity. Our current understanding of the biology of M. ptb infection has been hindered by limited knowledge of the host factors involved in the immune response to the organism and the lack of appropriate molecular tools to dissect the host–pathogen interaction. Recognition by the host of molecular patterns displayed by microbes is essential to development of an effective immune response. Pattern recognition receptors (PRRs) are the main sensors of pathogen and danger signals in innate immunity. They are mainly expressed by macrophages and dendritic cells of different organs. Toll like receptors (TLRs) are the most studied and best characterized PPRs which are responsible for sensing pathogen associated molecular patterns (PAMP). Recent studies have focused on the role of the TLRs family of cell membrane receptors in initiating cell signaling associated with mycobacterial infections. Activation of TLRs has also been shown to coordinate the adaptive immune response to microorganisms. In this study, we focused on the expression patterns of TLR2, TLR4 transcript in peripheral blood mononuclear cells (PBMC) of cows infected with M.ptb by Real-time quantitative PCR. Our results demonstrate a diffrential expression patterns of TLR2 and TLR4 in infected versus healthy cows which might have a potential implication in our undrestanding of the molecular pathogenesis and immunity of this micoorganism.

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