Study illustrates how N-methylation modifies immune responses in macrophages during L. pneumophila infection, suggesting an adaptive mechanism.
Legionella pneumophila is widely recognized as the principal organism responsible for Legionnaires’ disease. Modifications of surface-exposed lipopolysaccharide in L. pneumophila are key determinants of bacterial adaptation to host cells. Using a mutant strain deficient in N-methylation of legionaminic acid and fluorescence-based biophysical analyses, it was demonstrated that N-methyl groups linked to the acetimidoylamino group of legionaminic acid modulate the physicochemical properties of the bacterial cell surface and influence the interaction of L. pneumophila with macrophages. Loss of N-methyl groups reduced the efficiency of bacterial interaction with THP-1-derived macrophages and impaired intracellular proliferation. In addition, the presence of N-methyl groups in legionaminic acid contributes to increased TNF-α production in THP-1 macrophages stimulated with L. pneumophila sg1 LPS, without affecting IL-6 induction, suggesting that N-methylation of legionaminic acid may skew the early pro-inflammatory response toward TNF-α-dominated signaling during L. pneumophila infection.
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Kowalczyk et al. (2026) studied this question.
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