Transmission of commensal *Klebsiella michiganensis* resists Enterobacteraceae gut invasion

Intestinal microbiota contains beneficial microorganisms that protectagainst pathogen colonization. Antibiotics disrupt the microbiota andcompromise colonization resistance. Here, we determine how exchangingmicrobes between hosts impacts microbiota resilience against invaders’colonization post-antibiotic-induced dysbiosis. We assess functionalconsequences of dysbiosis using a mouse model of colonization resistanceagainst invading *Escherichia coli*. Antibiotics caused stochastic loss ofmicrobiota members, but co-housed animals’ microbiotas remained moresimilar to each other than those among singly housed animals. Strikingly,co-housed animals maintained colonization resistance post-antibiotics,whereas most singly housed mice were susceptible to *E. coli*. Retainingor sharing the commensal *Klebsiella michiganensis*, a member of the samefamily Enterobacteriaceae, was sufficient for colonization resistancepost-antibiotic-induced dysbiosis. *K. michiganensis *generally outcompeted *E.coli in vitro*, but *in vivo *administration of galactitol to bi-colonizedgnotobiotic mice, a nutrient supporting only *E. coli *growth abolished thecolonization resistance capacity of *K. michiganensis *against *E. coli*,supporting nutrient competition as the primary mechanism of interaction.*K. michiganensis *also hampered colonization of the pathogen *Salmonellaenterica* serovar Typhimurium, prolonging host survival. Our resultsaddress functional consequences of antibiotics stochastic effects, wherebymicrobial transmission through host interactions can facilitatereacquisition of beneficial commensals, minimizing the negative impact ofantibiotics.