Participation of the <i>Salmonella</i> OmpD Porin in the Infection of RAW264.7 Macrophages and BALB/c Mice

<div><p><i>Salmonella</i> Typhimurium is the etiological agent of gastroenteritis in humans and enteric fever in mice. Inside these hosts, <i>Salmonella</i> must overcome hostile conditions to develop a successful infection, a process in which the levels of porins may be critical. Herein, the role of the <i>Salmonella</i> Typhimurium porin OmpD in the infection process was assessed for adherence, invasion and proliferation in RAW264.7 mouse macrophages and in BALB/c mice. In cultured macrophages, a Δ<i>ompD</i> strain exhibited increased invasion and proliferation phenotypes as compared to its parental strain. In contrast, overexpression of <i>ompD</i> caused a reduction in bacterial proliferation but did not affect adherence or invasion. In the murine model, the Δ<i>ompD</i> strain showed increased ability to survive and replicate in target organs of infection. The <i>ompD</i> transcript levels showed a down-regulation when <i>Salmonella</i> resided within cultured macrophages and when it colonized target organs in infected mice. Additionally, cultured macrophages infected with the Δ<i>ompD</i> strain produced lower levels of reactive oxygen species, suggesting that down-regulation of <i>ompD</i> could favor replication of <i>Salmonella</i> inside macrophages and the subsequent systemic dissemination, by limiting the reactive oxygen species response of the host.</p></div>