SummaryHost−microbiota interaction plays fundamental roles in the homeostasis of mucosal immunity. Dysbiosis of intestinal microbiota has been demonstrated to participate in various immune responses and many multifactorial diseases. Study of intestinal microbiota has moved beyond the consequences of dysbiosis to the causal microbiota associated with diseases. However, studies of pulmonary microbiota and its dysbiosis are still in their infancy. Improvement of culture‐dependent and ‐independent techniques has facilitated our understanding of lung microbiota that not only exists in healthy lung tissue but also exerts great impact on immune responses under both physiological and pathological conditions. In this review, we summarize recent progresses of lung microbiota dysbiosis and its impact on the local immune system that determines the balance of tolerance and inflammation. We discuss the causal roles of pulmonary dysbiosis under disease settings, and propose that the interaction between lung microbiota and host is critical for establishing the immune homeostasis in lung.

Acquisition of nutrients from different species is necessary for pathogen colonization. Iron is an essential mineral nutrient for nearly all organisms, but little is known about how pathogens manipulate plant hosts to acquire iron. Here we report that AvrRps4, an effector protein delivered by Pseudomonas syringae bacteria to plants, interacts with and targets the plant iron sensor protein BRUTUS (BTS) to facilitate iron uptake and pathogen proliferation in Arabidopsis thaliana. Infection of rps4 and eds1 by P. syringae pv. tomato (Pst) DC3000 expressing AvrRps4 resulted in iron accumulation, especially in the plant apoplast. AvrRps4 alleviates BTS-mediated degradation of bHLH115 and ILR3(IAA-Leucine resistant 3), two iron regulatory proteins. In addition, BTS is important for accumulating immune proteins EDS1 at both the transcriptional and protein levels upon Pst (avrRps4) infections. Our findings suggest that AvrRps4 targets BTS to facilitate iron accumulation and BTS contributes to RPS4/EDS1-mediated immune responses.

Plasma membrane-localized receptor-like kinases (RLKs) perceive conserved pathogen-associated molecular patterns (PAMPs) in plants, leading to PAMP-triggered immunity (PTI). The Arabidopsis thaliana lectin RLK LecRK-IX.2 has been shown to regulate the bacterial flagellin-derived peptide flg22-induced PTI.Here, we discover that Pseudomonas syringae effector AvrPtoB targets LecRK-IX.2 for degradation, which subsequently suppresses LecRK-IX.2-mediated PTI and disease resistance. However, LecRK-IX.2 can interact with and phosphorylate AvrPtoB at serine site 335 (S335). AvrPtoB self-associates in vitro and in vivo, and the association appears to be essential for its E3 ligase activity in ubiquitinating substrate in plants. Phosphorylation of S335 disrupts the self-association and as a result, phosphomimetic AvrP-toB S335D cannot ubiquitinate LecRK-IX.2 efficiently, leading to the compromised virulence of AvrPtoB in suppressing PTI responses. flg22 enhances AvrPtoB S335 phosphorylation by inducing the expression and activating of LecRK-IX.2. Our study demonstrates that host RLKs can modify pathogen effectors to dampen their virulence and undermine their ability in suppressing PTI.