A General Perspective Of Microbiota In Human Health And .
Review ArticleiMedPub Journalswww.imedpub.comArchives of Clinical MicrobiologyISSN 1989-84362020Vol.11 No.2:106DOI: 10.36648/1989-8436.11.2.106A General Perspective of Microbiota in Human Health and DiseaseMbuvi P Mutua1*, Shadrack Muya2 and Gicheru M Muita11Departmentof Zoological Sciences, Kenyatta University, P.O Box 43844-00100, Nairobi, Kenya2Departmentof Zoology, Jomo Kenyatta University of Agriculture and Technology, P.O Box 62000-00200, Nairobi, Kenya*Correspondingauthor: Mbuvi P Mutua, Department of Zoological Sciences, Kenyatta University, P.O Box 43844-00100, Nairobi, Kenya, Tel:254727677738; E-mail: patmbuvi@gamil.comReceived date: February 03, 2020; Accepted date: February 18, 2020; Published date: February 27, 2020Citation: Mutua MP, Muya S, Muita G (2020) A General Perspective of microbiota in Human Health and Disease. Arch Clin Microbiol Vol. 11 No.2:106Copyright: 2020 Mutua MP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.AbstractThe study of human microbiome is widely perceived to bea young biomedical discipline. Recent studies indicate anassociation between human microbiome and chronicdisease conditions such as diabetes and obesity. Anunderstanding of human microbiome structure andfunction is important for design and delivery of microbialbased therapies especially against immunological andmetabolic chronic diseases. In this review, wedemonstrate the role human microbiota in health anddisease in various anatomic sites and in development ofneonate immunity. In particular, the review focuses onthe role of placental microbiota in fetoplacental unitreceptivity and the effect of early microbiota exposure onneonate immunity development. Additionaly, microbiotaimpact on health and disease in the gut, lung and skin isexplored.Keywords:Microbiota; Neonate; Dysbiosis; Pregnancy;Lungs; Skin; Gastrointestinal tractAbbreviations:AMP: Antimicrobial Peptides; IFN β: Interferon BetaIntroductionDysbiosis refers to compositional and functional changes ofthe microbiome and it can result into changes of all or any ofthe following microbiome characteristics: Microbiome stability,Microbiome diversity, and Microbiome resilience [1].Microbiome stability also referred to as microbiome resistanceis the amenability of microbiota to perturbations. Microbiomediversity refers to richness of the microbiota ecosystem.Microbiome resilience is the ability of microbiota to getrestored to pre-perturbation state. Dysbiosis can be driven byenvironmental and host related factors. However, variability ofmicrobiota among healthy individuals of different age,geographical limits and dietary habits, limits the definition ofwhat actually constitutes the dysbiotic state. In view of thislimitation, [1] have defined dysbiosis as a microbial communitystate that is not only statistically associated with disease, butalso functionally contributes to etiology, diagnosis, ortreatment of the disease.Literature ReviewDysbiotic state can fall in either of the following categories:(a) Decline of commensals which is either a reduction orcomplete loss of microbiota and can be caused by either directkilling of microbiota or attenuation of microbiota proliferation[2]. Loss of commensals has been observed in Clostridiumdifficile induced inflammation and restoration of thediminished Clostridium scindens has been reported toameliorate the inflammatory condition [3]. (b) Dysbiosis canalso result from growth of commensal microbiota that haspotential to cause pathology; such commensals have beenreferred to as pathobionts [4]. Studies report existence ofpathobionts at low relative abundance, but grow when there isimpairment of the microbial ecosystem. This type of dysbiosishas been observed in the Entero bacteriaceae, whose bloom iscommonly observed in enteric inflammation [3]. (c) Loss ofmicrobiota species diversity within a site, known as decline inalpha diversity, also constitutes dysbiosis and this type ofmicrobiota perturbation has been linked to metabolic health[5]. Alpha diversity in the intestinal microbiota increasesduring the first years of life and is a function of dietarypatterns [6]. Low intestinal bacterial diversity has beendocumented in AIDS, Intestinal bowel disease and type 1diabetes [7], and this has been attributed to abnormal dietarycomposition [8].Microbiota in pregnancyThe role of trophoblast cells in regulating immune activitiesat the maternal-fetal interface is well documented.Trophoblast cells can promote a tolerogenic phenotype, senseand respond to pathogen associated molecular patternspresent in microorganisms, and that a breach of thetrophoblast immunity can cause pregnancy complications Copyright iMedPub This article is available from: 10.36648/1989-8436.11.2.1061
Archives of Clinical MicrobiologyISSN 1989-8436including preterm birth [8,9]. Bacterial infections account formore than 40 % of preterm birth cases [10]. Infectious bacteriacan access maternal-fetal interface by descending fromperitoneal cavity, from maternal circulation or by ascendingfrom the lower reproductive tract [11]. Research findingsindicate that bacterial infections at the maternal-fetal interfaceweaken the trophoblast capacity to induce and promote nflammatory immune reactions with subsequent fetal loss[12]. Despite strong evidence linking bacterial infections topregnancy complications, antibiotic treatment has not proveneffective [13]. Recent studies demonstrate existence ofplacental microbiota to play a critical role in success ofpregnancy [14]. Escherichia coli and other Proteo bacteriafamily, have been shown to be abundant placental microbiome[15,16]. It is now documented that placental microbiotaactivities induce tolerogenic immunity, thereby permeatingreceptability and preventing rejection of fetal-placental unit[17]. Additionally, exposure of the fetus to maternalmicrobiota during pregnancy can significantly affectdevelopment of postnatal immunity in the neonate [18].Maternal-fetal interface microbiota improves trophoblastexpression of IFN β. IFN β modulate maternal immune systemwith increased maternal-fetal tolerance and receptivity [19].IFN β belong to type 1 IFNs that trigger programmed cell deathin activated T-cells and increase production ofimmunosuppressive molecules at the maternal-fetal interface[20]. Viruses inhibit type 1 IFN pathway in the trophoblast.Consequently, placental microbiota capability to induce animmunosuppressive, tolerogenic trophoblast type 1 IFNpathway can be abolished by viral infections [21]. Further, viralinfections shit placental microbiota milieu that has animmune-tolerant setting to a pro-inflammatory state [22].Neonate microbiota and disease developmentEarly life microbiota affects allergy development later inchild hood. Studies indicate low intestinal microbiota diversityduring the first month of life is associated with allergicsensitization and asthma in children aged 6-7 years [23].Colonization with Bifidobacterium breve is associated withreduced risk of atopic dermatitis in the first year of life butBifidobacterium catenulatum colonization is linked to a higherrisk of atopic dermatitis [24]. In a Canadian study of infants,low abundance of Faecalibacteria, Lachnospira, Veillonella andRothia genera at 3 months following parturition wasassociated with higher risk of asthma and allergy development[25]. In a study conducted in the US, infants with lowerabundance of species within Lactobacillus, Faecalibacteria,Bifidobacterium and Akkermansia genera at 1 month of agehad a higher chance of getting asthmatic attack at the age of 4years compared to those with higher abundance of the genera.The authors of the study suggested that long-termimmunological consequences of the specific early lifemicrobiota profiles could be exerted through production ofdistinct microbiota metabolites [26].22020Vol.11 No.2:106Skin microbiotaThe skin surface is a lipid and protein rich cornified layer,occasionally with invagination interruptions where follicles arelocated. The skin surface and follicles are both physically andchemically distinct [27,28]. The skin microbiota exhibitsspecific site distribution patterns with Cutibacterium andStaphylococcus predominantly residing in sebaceous areassuch the face and torso while Corynebacterium, betaProteobacteria and Staphylococcus dominating moist surfacessuch as the armpits [29]. This microbiota distribution patternindicates skin niche chemistry drives microbiome distribution[29]. Skin microbiota assembly process begins during birth [30]but the microbiota shifts notably during puberty, acterium and a decline in abundance of Firmicutes [31].However, in adulthood, skin microbiota remains stable overtime [32].Skin microbiota modulate the expression of various innatefactors such as the components of complement [33] andantimicrobial peptides (AMP) that are majorly in form ofcathelicidins and β-defensins. Cutibacterium stimulateproduction of AMP in keratinocytes and sebocytes [34] whileStaphylococcus epidermidis have been demonstrated toproduce AMP [35,36]. Corynebacterium microbial membersconstitute a major skin microbiota genus. Corynebacteriumand Mycobacteria genera share common microbiologicalfeatures such as similar surface and cellular structures. It is notyet clear how the skin immune system distinguishes betweenbacteria with such similar features [37]. Structurally,Corynebacterium cell wall has lipoglycans termed lipomannasand lipoarabinomannas both of which are ligands for the hostToll-like-receptors and C-type lectins. The binding of theligands and receptors triggers a pro or anti-inflammatoryresponse depending on the immunological context in whichthe ligand-receptor complex is sensed [38]). Recent studiesreport microbe-microbe interactions to impact on humanhealth. The skin microbiota Corynebacterium accolens inhibitsgrowth of Streptococcus pnuemoniae, a common respiratorytract pathogen [39]. This interaction is mediated bycorynebacterial lipase which hydrolyses triolein to release oleicacid which in turn inhibits pneumococcal growth [39]. Skinresident Staphylococcus epidermidis produce AMP that killStaphylococcus aureus and transplantation of Staphylococcusepidermidis into the skin of patients with atopic dermatitis isknown to decrease colonization by Staphylococcus aureus [36].Further, Staphylococcus epidermidis confer cutaneous immuneprotection against infections by activating keratinocytes toproduce AMP [40]. Therefore, skin microbiota immuneprotection goes beyond competitive exclusion.Lung microbiotaHistorically, the dogma that lung is a sterile organ has beenheld, however, in the last decade, studies have demonstratednew knowledge that the lung is not sterile and actually, theorgan harbors a diverse interacting microbiota [41,42].However, there is dearth of information regarding thepotential role of lung microbiota in regulation of lung immuneThis article is available from: 10.36648/1989-8436.11.2.106
Archives of Clinical MicrobiologyISSN 1989-8436response and homeostasis. The lung is incessantly exposed tomicrobiota either through inhalation or subclinical aspirationfrom birth [43]. According to a study [44], the lung is exposedto 7000 liters of diverse microbe rich air every day. The upperrespiratory tract where microbes are found in abundance is indirect communication with the lung and sub clinical aspirationof oropharyngeal microbial rich content occurs frequently inhumans [45,46]. The respiratory tract mucociliary systemensures a constant level of microbe immigration andelimination in the lung. Using a high-throughput sequencing ofamplicons of the 16s rRNA gene, a highly conserved locus inthe bacterial genome, a study [47] demonstrated that bacteriain healthy airways were similar but distinct from airways ofasthma patients, who predominantly had Proteobacteriaphylum. The major bacterial phyla in healthy lung reported byvarious studies are Bacteroidetes, and Firmicutes [47-49].There is relatively low bacterial biomass in the human lung.Human bronchoalveolar lavage studies have reported biomassfrom 4.5 to 8.25 log copies/Ml [50,51]. Newborns acquire skinmicrobiota that resembles their mothers ’ microbiome in amanner that is specific to the method of delivery. Infants bornby vaginal route acquire skin bacterial communities resemblingmothers ’ vaginal microbiota dominated by Lactobacillus,Sneathia or Prevotella, while those born by cesarean sectionacquire microbiota resembling that of mothers ’ skinmicrobiota composed of Corynebacterium, Cutibacterium andStaphylococcus species [52]. However, studies that haveexamined the dynamic changes that may occur in the lowerrespiratory tract microbiota during pregnancy and aschildhood progresses are scarce. In the lungs, conditions thataffect bacterial proliferation include oxygen tension, local pH,epithelial cells structure, blood flow and effector inflammatorycell profile [53,54]. Further chronic lung diseases mayconsiderably alter microbial community through elevatedvolumes of micro aspiration achieved by cough andmucociliary clearance [55]. A study [56], for instance, reportedincrease in abundance of Prevotella and Veillonella inlymphocyte and neutrophil mediated lung inflammation.Chronic lung diseases are characterized by interludes of acuteexacerbations marked by decline in pulmonary function andworsening pulmonary symptoms. Such exacerbations are themain cause of morbidity and mortality. Chronic lung diseaseexacerbations are indicative of disease progression and manypatients fail to restore to their pre-perturbation functional andphysiological state, a situation that has been associated withlung microbiota dysbiosis [57]. There is, for example, a declinein abundance of lung Bacteroidetes in asthmatic airways [47].In another study, lung Proteobacteria were the predominantmicrobiota found during bronchial hyper-responsiveness [58].Additionally, host microbiome interaction has been reportedas a critical aspect of asthma development. Children born withbroad lung microbial exposures were reported to be protectedfrom asthma and atopy [58]. Further, an association between ahigher fiber diet and reduced risk of asthma has beendemonstrated [59]. Copyright iMedPub2020Vol.11 No.2:106Gut microbiotaThe human gut harbors an estimated 1000 bacterial speciesand that, gut microbiota dysbiosis has been associated withmultifactorial disease conditions such as inflammatory boweldisease, obesity and type 2 diabetes interlia [60]. The gutmicrobiota of a healthy human confers a number of healthbenefits including pathogen protection, immune modulationand nutrition [61]. Following birth, the neonate gut is rapidlycolonized by microbiota and this has been reported to dependon mode of delivery, feeding type and use of antibiotics [62].Early gut microbial members include enterobacter andenterococci followed by anaerobic Bifidobacteria, clostridia,and Bacteroides species [63]. In the adult gut microbiota, thepredominant bacterial phyla reported are Firmicutes andBacteroidetes. Other phyla present in low abundance ndVerrucomicroba [64]. The butyrate producing bacteriaFaecalibacterium, Roseburia and Bacteroides have also beenidentified in a healthy human gut microbiota [65]. It has beendocumented that there is age related alterations in the gutmicrobiota of elderly people. In a study of people aged over 65years, the predominant gut microbiota was found to beBacteroidetes and this was associated with the low gradeinflammation, otherwise referred inflammaging, of thegastrointestinal tract in the elderly [66]. A number of diseaseshave been linked with gut dysbiotic state. In inflammatorybowel disease which is characterized by chronic and relapsinginflammation of the intestinal tract, gut dysbiosis has beenassociated with the development of mucosal lesions [67].Lower abundance of the Bacteroidetes and Firmicutes phylahas been reported in intestinal bowel disease [68].Additionally, the gut microbiota Roseburia needed for butyrateproduction and the Phascolarcto bacterium needed forsuccinate production are significantly low in intestinal boweldisease [69]. Several studies suggest a role of gut microbiota inthe pathogenesis of colorectal cancer [70,71]. It has beenreported that abundance of Fusobacteria to increase incolorectal cancer tumors compared to control samples [71]. ecrophorum and Fusobacterium mortiferum were enriched intumor tissue but there was decline in proportions ofFirmicutes and Bacteroidetes [71]. It is thought thatFusobacterium contribute to colorectal cancer pathogenesis byeliciting tumor inflammation [72]. Irritable bowel syndrome,marked by abdominal pain and altered bowel habits, gutdysbiosis has been associated with the disease low gradeintestinal inflammation [73]. Further, gut dysbiotic state hasbeen suggested to facilitate pathogen adhesion in irritablebowel syndrome [74]. In irritable bowel syndrome, there isconsiderable increase in abundance of Firmicutes,Ruminococcus, Clostridium, and Dorea and a decline inproportions of Bifidobacterium and Faecalibacterium species[75]. There is paucity of information regarding associationbetween gut microbiota and obesity. However, a study [60]established a decrease in the ratio of Firmicutes toBacteroidetes following weight loss in human subjects. Inanother study, a lower proportion of Bacteroidetes in obeseindividuals but increased abundance of Actinobacteria with a3
Archives of Clinical MicrobiologyISSN 1989-8436fairly stable proportion of Firmicutes was reported. In type 2diabetes, which is principally linked with obesity related insulinresistance, there is low proportion of Firmicutes but a higherproportion of Bacteroidetes compared to normal controls.Further, type 2 diabetes patients have a gut dysbiosis with ahigher proportion of opportunistic pathogens such asClostridium species but a lower proportion of butyrateproducing bacteria [65].ConclusionThe human microbiome plays a critical role in human healthand disease. Resident microbiota in different anatomic sites ofhuman body influence metabolism, physiology and modulateimmune system development. Perturbation of microbiota isassociated with several multifactorial disease conditions andthis is fundamental in development of appropriate therapeuticapproaches. Targeting of specific constituents of microbiotamay potentially permeate removal of harmful microorganismsand or their metabolites and enrichment of beneficialmicrobes.DeclarationsCompeting interestsThe authors declare that they have no competing interests.FundingWe thank Louise Bowditch who provided funds for thisreview.Authors’ contributionsMPM wrote the manuscript. MSh and GM providedadditional information, read and improved the manuscript.AcknowledgementsNot applicable.Competing interestsThe authors declare that they have no competing interests.References1.2.3.4Maayan L, Aleksandra A, Kolodziejczyk AA, Thaiss CA, Elinav E(2017) Dysbiosis and the immune system. Nat Rev Immunol 4:219-232.Krem T, Zeevi D, Suez J, Weinberger A, Avnit-Sagi T, et al. (2015)Growth dynamics of gut microbiota in health and diseaseinferred from single metagenomics samples. Science 349:1101-1106.Buffie CG, Bucci V, Stein RR, McKenney PT, Ling L, et al. (2015)Precision microbiome reconstitution restores bile acid mediatedresistance to Clostridium difficile. Nature 517:205-208.2020Vol.11 No.2:1064.Stecher B, Maier L, Hardt WD (2013) “Blooming” in the gut: howdysbiosis might contribute to pathogen evolution. Nat RevMicrobiol 11: 277-284.5.Chow J, Mazmanian SK (2010) A pathobiont of the microbiotabalances host colonization and intes
A General Perspective of Microbiota in Human Health and Disease Mbuvi P Mutua1*, Shadrack Muya2 and Gicheru M Muita1 1Department of Zoological Sciences, Kenyatta University, P.O Box 43844-00100, Nairobi, Kenya 2Department of Zoology, Jomo Kenyatta University of Agriculture and Technology, P.O Box 62000-00200, Nairobi, Kenya *Corresponding author: Mbuvi P Mutua, Department of Zoological .
Faecal microbiota transplantation from donors with a normal microbiota effectively . A consistent metabolic signature was identified in the post-transplant microbiota, with reduced primary . the ratio of inflammatory to non-inflammatory FAs decreased. Keywords: Clostridioides difficile, Faecal m
of the gut microbiota. Tilg et al. recently reported a dir-ect link between altered microbiota composition and the inflammatory status of patients with type 2 diabetes; decreased diversity of the intestinal microbiota may lead to a failure to maintain the intestinal barrier needed to prevent systemic dissemination of gut bacteria and asso-
that the ileal mucosa-associated microbiota underwent major changes following surgery with differences between patients with or without endoscopic recurrence. Moreover, endoscopic recurrence was associated by itself with alteration in the gut microbiota. Finally, using several strategies, we showed that the gut microbiota at the time of surgery .
Diet‑linked changes in the ileal microbiota Ileal microbiota richness and structure were not signi-cantly dierent when comparing the LP and HP groups at any time point (P 0.05). When considering both dietary groups, the ileal microbiota destabilised after weaning and the transition to solid feed only (P 0.036).
tinal microbiota. Changes in the dietary structure lead to the occurrence and development of metabolic diseases by affect-ing the composition and function of intestinal microbiota. For example, alterations in intestinal microbiota inhibit the transformation of bile acid in the lipid and glucose metabo-lism disturbance induced by a high-fat .
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The Gut Microbiota Human gut is home to 100 trillion bacterial cells Density of 1011 to 1012 per gram in the colon weighing 2kg Genome size of microbiota at least 100-fold greater than human Large numbers species present (200-1000 species), most uncultured Nat. Rev. Micro. 2011;9:279-290 The Human MicrobiomeFile Size: 1MB
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