Alterations in Oral–Nasal–Pharyngeal Microbiota and Salivary Proteins in Mouth-Breathing Children

Abstract

Mouth breathing induces a series of diseases, while the influence on microbiota of oral cavity and salivary proteins remains unknown. In this study, for the first time, profiles of oral–nasal–pharyngeal microbiota among mouth-breathing children (MB group, n = 10) were compared with paired nose-breathing children (NB group, n = 10) using 16S ribosomal DNA (rDNA) (V3–V4 region) high-throughput sequencing. The differentially expressed salivary proteins were revealed using label-free quantification (LFQ) method, and their associations with bacterial abundance were measured by canonical correspondence analysis (CCA). The overall bacterial profiles differed between the two groups, and the differences were related to the duration of mouth breathing. The diversity of oral–pharyngeal microbiota was significantly higher, and the nasal–pharyngeal species tended to be consistent (unweighted UniFrac, p = 0.38) in the MB group. Opportunistic pathogens were higher in relative abundance as follows: Acinetobacter in the anterior supragingival plaque, Neisseria in unstimulated saliva, Streptococcus pneumoniae in the pharynx, and Stenotrophomonas in the nostrils. The expression level of oxidative-stress-related salivary proteins (lactoylglutathione lyase and peroxiredoxin-5) were upregulated, while immune-related proteins (integrin alpha-M and proteasome subunit alpha type-1) were downregulated in MB group. The differentially expressed proteins were associated with specific bacteria, indicating their potentials as candidate biomarkers for the diagnosis, putatively early intervention, and therapeutic target of mouth breathing. This study showed that mouth breathing influences the oral–nasal–pharyngeal microbiota and enriches certain pathogens, accompanied with the alterations in the salivary environment. Further research on the pathological mechanisms and dynamic changes in longitudinal studies are warranted.

Life and death of a leprosy sufferer from the 8th-century-CE cemetery of Kiskundorozsma–Kettőshatár I (Duna-Tisza Interfluve, Hungary)—Biological and social consequences of having Hansen’s disease in a late Avar Age population from Hungary

“…Because of the persistent blockage of his nasal airways, the middle-aged male could have experienced difficulties in breathing through his nose; and thus, he could have developed an oral breathing habit that is a frequent accompaniment of lepromatous leprosy [44,49,50]. As oral breathing can contribute to changes in the intraoral humidification, pH, and oxygen levels, it can have a negative impact on oral health [51]. For instance, chronic oral breathing can increase the risk of developing periodontitis, dental calculus or caries [51,52].…”

The Influence of Diet on Oxidative Stress and Inflammation Induced by Bacterial Biofilms in the Human Oral Cavity

“…Low and high levels of oxidative stress mobilize cellular antioxidant mechanisms and stimulate the inflammatory response of cells, but very high levels of oxidative stress contribute to cell death (apoptosis and necrosis). A positive thing in this situation is the fact that maintaining an appropriate level of oxidative stress significantly influences the treatment of many inflammatory diseases [ 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 ,…”

“…On the one hand, the knowledge of the biological properties of reactive oxygen and nitrogen species helps to predict potential dangers in certain disease states. On the other hand, the knowledge of natural antioxidant mechanisms and their use, as well as their support by pharmacological substances neutralizing their negative derivatives, as well as the ability to cope with everyday stress, can be an effective support in the treatment of periodontal diseases in disease states [ 14 , 15 , 16 , 29 , 33 , 36 , 56 , 63 , 78 , 81 , 93 , 97 , 99 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 ].…”

“…The pathognomonic lesion of the periodontium is the periodontal pocket and the modulation of inflammation in the periodontal pocket itself. The modern pathogenetic model of genes, proteins and metabolites in dynamic biological processes is based on a multi-level structure that includes disease initiation and eradication mechanisms, regulated by innate and environmental factors [ 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 ,…”

Respiratory and Neurological Disease across Different Ethnic Groups Is Influenced by the Microbiome

“…The classifier identified African Americans with a 100% sensitivity and 74% specificity and Caucasians with a 50% sensitivity and 91% specificity signifying that our microbiome may be genetically influenced and can act as an ethnic fingerprint [ 55 ]. Although nasal and oral microbiota have obvious discrepancies due to distinct environments for bacterial adhesion, survival, and growth [ 56 ], the differences observed are broadly mirrored disparities in each taxon’s signal abundance at each site. Since both the oropharynx and nostril collect drainage from shared sources (nasopharynx, sinuses, and nasal cavity), there is a major overlap in the taxa seen [ 57 ].…”