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Lipopolysaccharide is an essential macromolecule that comprises the outer surface of gramnegative bacteria. Lipopolysaccharide, recognized by the human host as a foreign molecule, elicits an immune response that is designed to eliminate the bacterial intruder. Lipopolysaccharide from enteric bacteria such as Escherichia coli provokes a strong immune response. On the molecular level this is because E. coli lipid A, the bio-active component of lipopolysaccharide, is a strong agonist of the innate immune receptor, Tolllike receptor 4 (TLR4). However, lipopolysaccharide from the periodontopathogen, Porphyromonas gingivalis, elicits a strikingly weak immune response. Additionally, P. gingivalis is capable of synthesizing a heterogeneous population of lipid A molecules, which are subtly different from each other in structure. One of these lipid A structures has the capacity to dampen the immune response elicited by lipid A agonists at TLR4. The weak agonistic and antagonistic lipid A structures of P. gingivalis are proposed to play an important role in disrupting the oral immune homeostasis required for maintaining oral health, and thereby promote periodontal disease.
Jain et al. (Mon,) studied this question.
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