Stomata are entry sites for bacterial pathogens and can affect the outcome of infection to the disadvantage of the pathogen. This is referred to as stomatal immunity. Guard cells can mediate certain responses in a cell-autonomous manner, but this question remains to be addressed for pathogen-induced stomatal closure. This study reports transient and stable transgenic approaches to study guard cell responses. I employed virus-induced gene silencing and guard cell-specific promoters to investigate guard cell autonomy and non-autonomous signalling events during pathogen-induced stomatal closure. Plants that express FLAGELLIN SENSING 2 (FLS2) only in the guard cells retained stomatal closure to flg22 and wild-type-like susceptibility levels to bacterial infection. Interestingly, guard cell-specific knock-down of FLS2 did not impair stomatal closure or resistance to bacteria, suggesting that non-autonomous signalling events can mediate stomatal closure during pathogen invasion. Screening mutants of abscisic acid (ABA) signalling components revealed that pathogen-induced stomatal closure is independent from the prototypic drought stomatal closure pathway. I showed that OPEN STOMATA 1 is not involved in pathogen-induced stomatal closure and that it was inactive after flg22 treatment. Instead, the mutant of a related kinase SUCROSE NON-FERMENTING RECEPTOR KINASE 2.3 (SnRK2.3) was impaired in its flg22 stomatal closure response suggesting that SnRK2.3 plays an important role in this response. SnRK2.3 interacted with BOTRYRIS-INDUCED KINASE 1 in split-YFP and co-immunoprecipitation assays. Interestingly, the PBS1-like 1 (PBL1) mutant was impaired in flg22-induced stomatal closure and PBL1 activated SLOW ANION CHANNEL-ASSOCIATED 1 HOMOLOGUE 3 (SLAH3) in oocyte measurements. This suggests PBL1 as major player in MAMP-induced stomatal closure. My data reveal that aspects of stomatal immunity involve both guard cell-specific signalling events and non-symplastic cell-to-cell signalling. This work implicates independence of ABA- and pathogen-induced stomatal closure pathways and PBL1 as major regulator through direct activation of the anion channel SLAH3.