Intestinal microbiota contains beneficial microorganisms that protect
against pathogen colonization. Antibiotics disrupt the microbiota and
compromise colonization resistance. Here, we determine how exchanging
microbes between hosts impacts microbiota resilience against invaders’
colonization post-antibiotic-induced dysbiosis. We assess functional
consequences of dysbiosis using a mouse model of colonization resistance
against invading *Escherichia coli*. Antibiotics caused stochastic loss of
microbiota members, but co-housed animals’ microbiotas remained more
similar 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*. Retaining
or sharing the commensal *Klebsiella michiganensis*, a member of the same
family Enterobacteriaceae, was sufficient for colonization resistance
post-antibiotic-induced dysbiosis. *K. michiganensis *generally outcompeted *E.
coli in vitro*, but *in vivo *administration of galactitol to bi-colonized
gnotobiotic mice, a nutrient supporting only *E. coli *growth abolished the
colonization 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 *Salmonella
enterica* serovar Typhimurium, prolonging host survival. Our results
address functional consequences of antibiotics stochastic effects, whereby
microbial transmission through host interactions can facilitate
reacquisition of beneficial commensals, minimizing the negative impact of
antibiotics. Less...