In this study, we highlight that
S. warneri is a natural member of the human adult gut microbiota with a prevalence of ~ 34% in a population of healthy individuals. Interestingly, we also detected
S. warneri in the mouse gut microbiota, thereby confirming previous observations of this bacterium in fecal samples from other mammals [
26‐
30]. Together, these results suggest that
S. warneri is a common member of mammal gut microbiota.
The ability of
Staphylococcus species to invade human cells has most often been studied with
S. aureus, which can invade various cell lines such as endothelial cells, epithelial cells, keratinocytes and osteoblasts [
31]. This host cells invasion allows
S. aureus to escape host humoral immune responses, avoid shear stress-induced clearance and evade antibiotic activities.
S. aureus survival in nonphagocytic cells thus facilitates bacterial persistence and promotes chronic infections. Internalization of
Staphylococcus non-
aureus species in human cells has also been reported for
Staphylococcus lugdunensis [
11,
32,
33]
, Staphylococcus saprophyticus [
34,
35],
Staphylococcus pseudintermedius [
36],
Staphylococcus delphini [
37] and
S. epidermidis [
8‐
11], which have been classically considered as opportunistic pathogens [
6]. Pathogenic CoNS species are responsible for foreign body-related infections as well as infections in preterm newborns [
6]. Colonization of the skin and mucosa by these bacteria may constitute an important source of endogenous infections. These bacteria can indeed switch between the nonpathological colonization of body surfaces to infections and uncontrolled replication owing to decreases in host immune surveillance (for example in immunocompromised individuals) or breaches in the skin or mucosal barriers (for example during the insertion of catheters or implantation of orthopedic devices). Some clinical cases of bloodstream infections by
S. epidermidis in adults or in preterm neonates showed that genetically similar
S. epidermidis strains were present in the gut of these patients, which may thus constitute the source of infection [
38,
39]. In contrast to
S. epidermidis, only a few cases of
S. warneri infections have been reported, suggesting its lower pathogenic potential. Our results, which show that
S. warneri can invade enterocytes, raise the question of the consequences of these internalization events on intestinal physiology. It would particularly be interesting to decipher whether these internalization events trigger local inflammation in response to the detection of the bacteria by the innate immune system, or promote the translocation of
S. warneri across the intestinal barrier, thereby facilitating infection in deeper tissues. Another possibility would be that the internalization of
S. warneri by intestinal cells constitutes a yet uncharacterized type of mutualistic interaction between human cells and gut bacteria.