β‐Defensin Gene Expression during the Course of Experimental Tuberculosis Infection

Abstract

The kinetics of gene expression and the cellular source of murine beta -defensin-3 (mBD3) and murine beta -defensin-4 (mBD4) were determined in mouse models of progressive pulmonary tuberculosis and latent infection induced by high or low infecting doses, respectively. During progressive disease, there was an initial rapid expression of both defensins by respiratory epithelial cells that correlated with temporary control of bacillary proliferation, but expression decreased during the later progressive phase of the disease. In latent infection, both defensins were expressed continuously, but they were suppressed after reactivation of the disease. Thus, mycobacterial infection induces the expression of mBD3 and mBD4, and both might participate in the control of mycobacterial growth.

Mycobacterium boviswith different genotypes and from different hosts induce dissimilar immunopathological lesions in a mouse model of tuberculosis

“…We also studied the expression of mBD-4 as a significant factor of innate immunity. In this animal model, when infected with M. tuberculosis, H37Rv mBD-4 seems to have a significant role in the control of bacillary growth [20]. Interestingly, infection with either 04-303 or 04-302 induced very low mBD-4 expression, whereas the control strain AN5 induced progressively increasing expression of this anti-microbial peptide, peaking at day 120 (Fig.…”

“…In this animal model, we have shown that after infection with strain M. tuberculosis H37Rv there is rapid and high expression of mBD-4 during the early phase, while there is efficient control of bacillary replication. Then, during the progressive phase, there is a pronounced decrease in expression of mBD-4, while proliferation of the bacilli increases [20]. Thus, the low expression of mBD-4 in mice infected with highly virulent M. bovis strains could contribute to a high rate of bacillary replication and extensive tissue damage.…”

“…Different polymorphic MIRU loci ( MIRUs 2,4,10,16,20,23,24,26,27,31,39 and 40) were amplified with the oligonucleotides described previously [19]. The amplification mix consisted of 1¥ buffer (10 mM Tris-HCl, pH 9·0; 50 mM KCl, 0·1% Triton X-100) supplemented with Q buffer (Qiagen, GmbH, Hilden, Germany), 0·25 mM of each 2′-deoxynucleosides 5′-triphosphate, 0·1 mM of each primer and 1·25 U Taq polymerase (Hot Star; Qiagen …”

“…The experimental BALB/c model of progressive pulmonary tuberculosis has been described in detail previously [13,[20][21][22][23]. Briefly, bacillary suspensions were adjusted to 2·5 ¥ 10 5 viable cells in 100 ml phosphate-buffered saline.…”

The Role of Non-Phagocytic Cells in Mycobacterial Infections

“…CRAMP expression was high in the progressive phase of the disease and the protein was observed in different structures of the mycobacteria. The authors of these studies conclude that both defensins and cathelicidin participate in mycobacterial containment, not only by the direct activity against the bacteria, but by their recognized chemotactic activity (Rivas-Santiago et al, 2006;Castañeda-Delgado et al, 2010). Another antimicrobial peptide involved in the defense against M. tuberculosis is hepcidin.…”