Recognition ofStaphylococcus aureusby the Innate Immune System

Abstract

The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus

Staphylococcus aureus protein A induced inflammatory response in human corneal epithelial cells

“…The ability of epithelial cells to recognize and to respond to S. aureus infection in the cornea is related to the action of TLRs and MyD88. TLR2 recognizes a broad spectrum of pathogen associated molecular patterns (PAMPs) including PGN, LTA and lipoproteins derived from Gram-positive bacteria [16]. The interaction of TLRs with its PAMP results in the activation of multiple intracellular signaling events such as NF-κB activation and subsequent production of cytokines such as IL-6, IL-8, and TNF-α [2].…”

Airway epithelial cell signaling in response to bacterial pathogens

“…1). [1][2][3][4][5] Unlike other mucosal surfaces, the lower airways are normally sterile and exposure to bacterial components triggers an inflammatory response. Airway epithelial cells are polarized, form tight junctions and have a compartmentalized distribution of surface receptors.…”

“…Under unstimulated conditions, these receptors are expressed at low density on the cell surface which is likely to prevent excessive responses that impede normal lung function. However, upon repeated bacterial stimulation more 1 receptors are recruited to the apical surface where they initiate the inflammatory response when this is required to clear the infection. 5,6 Toll Like Receptors Among the eleven Toll like receptors (TLRs) that have been recognized to date, 7,8 TLRs 1-10 are expressed in airway epithelia.…”

Noninvasive Optical Imaging of Staphylococcus aureus Bacterial Infection in Living Mice Using a Bis-Dipicolylamine-Zinc(II) Affinity Group Conjugated to a Near-Infrared Fluorophore

“…For example, the plasma membrane which surrounds the Gram-positive bacterium Staphylococcus aureus is composed of approximately 75% anionic phosphatidylglycerol. Extending from this membrane are anionic glycerophosphate polymers called lipoteichoic acids, that weave through and anchor the surrounding peptidoglycan cell wall (14). Gram-negative bacteria such as Escherichia coli are differentiated by the presence of a second outer bilayer membrane.…”