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1 role of the hyphal form during vaginal human commensalism.
2 mptomatic carrier state similar to bacterial commensalism.
3 nisms other than altering lipid A to support commensalism.
4  acquiring branched-chain amino acids during commensalism.
5 ear to be a determinant for C. jejuni during commensalism.
6 ic host cells to promote pathogenesis and/or commensalism.
7 cues the inability of mutants to compete for commensalism.
8 uestion of how these molecules contribute to commensalism.
9  the yeast-to-hypha morphogenesis program on commensalism.
10 ion to the changing intestinal milieu during commensalism.
11 istic interactions-for example, mutualism or commensalism.
12 contributes to the maintenance of gut fungal commensalism.
13 een fungi and the immune system that promote commensalism.
14 ve resilience and a shift from antagonism to commensalism.
15 zf1, and Efg1 in vivo, that we show promotes commensalism.
16  the host intestine and repurposed to direct commensalism.
17 R4, AHR1, CZF1, and SSN6, also influence gut commensalism.
18 ition (10% of cases) to host-parasite (77%), commensalism (12%), and mutualism (1%).
19 lutionary and immune processes that underpin commensalism(2,3).
20 competition, commensalism and concurrence of commensalism and competition have been considered.
21      In this study, neutralism, competition, commensalism and concurrence of commensalism and competi
22  is likely to play an important role in both commensalism and dissemination to cause invasive disease
23  cause phenotypes to shift from mutualism to commensalism and even parasitism.
24 cosal surfaces, where it regulates microbial commensalism and excludes luminal factors from contactin
25 uable model organism for studying gut fungal commensalism and immunity in its native host.
26 blishment and maintenance of host-microbiota commensalism and immunity to pathogenic microorganisms.
27 l colonization of avian and animal hosts for commensalism and infection of humans for diarrheal disea
28                                  During both commensalism and infection, it must match the immunologi
29 tation, and cell wall remodelling, influence commensalism and infection.
30 tinct genetic programs to transition between commensalism and invasive pathogenesis.
31 ial binding to host receptors underlies both commensalism and pathogenesis.
32   Our findings indicate that many aspects of commensalism and pathogenicity are intertwined and that
33 ral mutation that alters the balance between commensalism and pathogenicity.
34 ria gonorrhoeae, straddle the border between commensalism and pathogenicity.
35  helps us to understand the origins of human-commensalism and the pace and form of adaptation to anth
36 ing that the protein is associated with both commensalism and the pathogenesis of disease.
37  tradeoff between fungal programs supporting commensalism and virulence in which selection against hy
38 ns including not only domestication but also commensalisms and mutualisms.
39 tory IgA immunity, the regulation of mucosal commensalism, and defense of the barrier against enterop
40 people in the north-from predation, probable commensalism, and taming, to domestication-and of their
41 t and its intestinal microflora that lead to commensalism are unclear.
42 rmining whether antagonisms, mutualisms, and commensalisms are equally common ecological strategies r
43                        Here, we define human-commensalism as a population-level dependence on anthrop
44 omal cell interaction in itself is a form of commensalism, because it has been demonstrated that thes
45  play a role in regulating intestinal fungal commensalism by coating fungal morphotypes linked to vir
46  enforcing mucosal tolerance and maintaining commensalism by promoting intestinal Treg cell formation
47 om competition to facilitation (for example, commensalism, cooperation and mutualism).
48 fitness, we also identify a set of candidate commensalism effectors.
49                        In addition, frequent commensalism generates CD25(hi) (Tregs) which modulate m
50                                        Human-commensalism has been intuitively characterised as an in
51                                              Commensalism implies a hitchhiking role for viruses-self
52 tion strategies C. jejuni employs to achieve commensalism in a natural host.
53 cterial requirements necessary for promoting commensalism in a vertebrate host.
54 EtN by EptC is key to its ability to promote commensalism in an avian host and to survive in the mamm
55                                   To promote commensalism in animals and disease in humans, Campyloba
56        Here we design an orthogonal obligate commensalism in Escherichia coli that autonomously creat
57  C. albicans and suggests that selection for commensalism in humans does not result in a fitness cost
58                 This mechanism occurs during commensalism in poultry to alter the colonization capaci
59                          During infection or commensalism, induction of IL-10 by B. fragilis is criti
60                                              Commensalism is critical to a healthy Th1/Th2 cell balan
61 on in suppressing autoimmunity and enforcing commensalism is established, a broader role for regulato
62             The current dogma of C. albicans commensalism is that the yeast form is optimal for gut c
63 he host controls mucus barrier integrity and commensalism is unclear.
64 fer from those employed for symbiosis during commensalism is unknown.
65 ng in the states of symbiosis, colonization, commensalism, latency, and disease.
66 lthy individuals, suggesting that pathobiont commensalism may elicit host benefits.
67 ction of antimicrobial lipids and restricted commensalism of Gram-positive bacterial communities.
68 ains of CiaI were analysed for importance in commensalism or invasion.
69 ion shifted an interaction from mutualism to commensalism or parasitism depended on whether the nutri
70 mutualism is likely in P-limited systems and commensalism or parasitism is likely in N-limited system
71  relationships encompass obligate mutualism, commensalism, parasitism, and pathogenicity.
72 d by wild animals, are most likely shaped by commensalism related to human activities.
73 intact barriers, but regulation of microbial commensalism remain largely unexplored.
74                                   Successful commensalism requires dampening of the inflammatory resp
75 on in mouse models of systemic infection and commensalism, respectively.
76         However, a clear definition of human-commensalism, rooted within an ecological and evolutiona
77              Phoresy is a widespread form of commensalism that facilitates dispersal of one species t
78  in understanding the evolution of brown rat commensalism, their global dispersal, and mechanisms und
79  albicans colonized mice, competitive fungal commensalism thereby mitigated fatal candidiasis.
80 n skin-resident ILCs that regulate microbial commensalism through sebaceous gland-mediated tuning of
81 tic mechanism leading to the transition from commensalism to a pathogenic lifestyle.
82 sh and their worms can shift from parasitism/commensalism to mutualism as crayfish age.
83 estication timelines, spanning antagonism to commensalism to mutualism.
84               Evidently, the transition from commensalism to opportunism in S. aureus does not requir
85 tress may be caused by a shift from apparent commensalism to parasitism in the corallicolid-coral hos
86  review, we will discuss the transition from commensalism to pathogenesis, the key players of the fun
87 obligatory endosymbiosis and from restricted commensalism to semi-parasitism, with the specialisation
88 en; however, how Candida albicans shift from commensalism towards a pathogenic status remains poorly
89                               The concept of commensalism was introduced 145 years ago.
90 investigate E. faecalis factors required for commensalism, we identified E. faecalis genes that are u
91     To understand how the bacterium promotes commensalism, we used signature-tagged transposon mutage
92 coordinated Treg-IgA response is to maintain commensalism with the microbiota.
93  microflora and the immune system to promote commensalism within the gut.
94        Our results reveal competitive fungal commensalism within the intestinal microbiota, independe