downregulates RECK to promote matrix metalloproteinase-9 secretion by bronchial epithelial cells.

Airway epithelial cells function as both a physical barrier against harmful substances and pathogenic microorganisms and as an important participant in the innate immune system. Matrix metalloproteinase-9 (MMP-9) plays a crucial role in modulating inflammatory responses during respiratory infections. However, the signalling cascade that induces MMP-9 secretion from epithelial cells infected with remains poorly understood.

T-B cell epitope peptides induce protective immunity against Mycoplasma pneumoniae respiratory tract infection in BALB/c mice.

Mycoplasma pneumoniae is the most common pathogen of community-acquired pneumonia in humans. Due to its high rates of antibiotic resistance, vaccination has become the best method to control the dissemination of M. pneumoniae.

Infection strategies of mycoplasmas: Unraveling the panoply of virulence factors.

Mycoplasmas, the smallest bacteria lacking a cell wall, can cause various diseases in both humans and animals. Mycoplasmas harbor a variety of virulence factors that enable them to overcome numerous barriers of entry into the host; using accessory proteins, mycoplasma adhesins can bind to the receptors or extracellular matrix of the host cell. Although the host immune system can eradicate the invading mycoplasma in most cases, a few sagacious mycoplasmas employ a series of invasion and immune escape strategies to ensure their continued survival within their hosts.

Subversion of the Immune Response by Human Pathogenic Mycoplasmas.

Mycoplasmas are a large group of prokaryotes which is believed to be originated from Gram-positive bacteria via degenerative evolution, and mainly capable of causing a wide range of human and animal infections. Although innate immunity and adaptive immunity play crucial roles in preventing mycoplasma infection, immune response that develops after infection fails to completely eliminate this bacterium under certain circumstances. Thus, it is reasonable to speculate that mycoplasmas employ some mechanisms to deal with coercion of host defense system.

HO-1 mediates the anti-inflammatory actions of Sulforaphane in monocytes stimulated with a mycoplasmal lipopeptide.

Exposure to Mycoplasma pneumoniae leads to lung inflammation through a host defense pathway. Increasing evidence has indicated that the mycoplasma-derived membrane lipoprotein, or its analogue macrophage-activating lipopeptide-2 (MALP-2), excretes LPS as an immune system-stimulating substance and plays a crucial role in pathological injury during M. pneumoniae infection.