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Toll‑like receptor 2 (TLR2) has been identified as a sensor for bacterial lipoprotein. To determine the role of TLR2 in host defense against Acinetobacter baumannii infection, wild‑type (WT) and TLR2‑deficient mice were infected intranasally with A. baumannii. Body weight, cytokine and chemokine levels in bronchoalveolar (BAL) fluid and lung histopathology were examined. Body weight changes in TLR2‑deficient mice were comparable to those of WT mice throughout the experimental period. However, TLR2‑deficient mice exhibited an increased bacterial load in the lungs and increased levels of interleukin‑6 and chemokine (C‑X‑C motif) ligand 2 in BAL fluids compared with WT mice 1 day after infection. Histopathological features of lung tissue in WT and TLR2‑deficient mice were comparable between WT and TLR2‑deficient mice. Results of the present study demonstrate that TLR2 may have a minimal role in the host defense against A. baumannii at the early stages of infection.

Periodontitis is a progressive chronic inflammatory disease and a major cause of tooth loss in humans. As a withanolides, withaferin A (WA) is known to exhibit strong anti‑inflammatory activity. The present study examined whether WA inhibited inflammatory responses in macrophages in response to two representative periodontal pathogens, Fusobacterium nucleatum and Aggregatibacter actinomycetemcomitans. Murine bone marrow‑derived macrophages (BMDMs) were used in this study and cytokine production in culture supernatants was measured by enzyme‑linked immunosorbent assays. Western blot analysis was performed to determine the activation of nuclear factor‑κB and mitogen‑activated protein kinases (MAPKs) and the expression of inducible nitric oxide synthase (iNOS), toll‑like receptor (TLR) 2 and TLR4. The production of nitric oxide (NO) was determined by the Griess reaction. WA treatment was shown to decrease interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α production in BMDMs in response to F. nucleatum and A. actinomycetemcomitans in a dose‑dependent manner. The phosphorylation of IκB‑α and MAPKs (p38, extracellular signal‑regulated kinases and c‑Jun N‑terminal kinases) induced by F. nucleatum and A. actinomycetemcomitans was also inhibited by WA. F. nucleatum and A. actinomycetemcomitans induced iNOS expression and NO production in BMDMs, which was inhibited by WA in a dose‑dependent manner. WA also reduced endogenous and induced expression of TLR2 and TLR4 in these cells. These results suggest that WA may be a potential therapeutic agent or preventive additive for periodontitis control.