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The bronchioles (/ ˈ b r ɑː ŋ k i oʊ l s / BRONG-kee-ohls) are the smaller branches of the bronchial airways in the lower respiratory tract.They include the terminal bronchioles, and finally the respiratory bronchioles that mark the start of the respiratory zone delivering air to the gas exchanging units of the alveoli.
A bronchus (/ ˈ b r ɒ ŋ k ə s / BRONG-kəs; pl.: bronchi, / ˈ b r ɒ ŋ k aɪ / BRONG-ky) is a passage or airway in the lower respiratory tract that conducts air into the lungs.The first or primary bronchi to branch from the trachea at the carina are the right main bronchus and the left main bronchus.
Bronchial hyperresponsiveness (or other combinations with airway or hyperreactivity, BH used as a general abbreviation) [1] is a state characterised by easily triggered bronchospasm (contraction of the bronchioles or small airways). Bronchial hyperresponsiveness can be assessed with a bronchial challenge test.
It arises above the level of the right pulmonary artery, and for this reason is named the eparterial bronchus. [1] All other distributions falling below the pulmonary artery are termed hyparterial . The eparterial bronchus is the only secondary bronchus with a specific name apart from the name of its corresponding lobe.
[3] There are ten bronchopulmonary segments in the right lung: three in the superior lobe, two in the middle lobe, and five in the inferior lobe. Some of the segments may fuse in the left lung to form usually eight to nine segments (four to five in the upper lobe and four to five in the lower lobe.
[1] The left bronchial arteries (superior and inferior) usually arise directly from the thoracic aorta. [2] The single right bronchial artery usually arises from one of the following: 1) the thoracic aorta at a common trunk with the right 3rd posterior intercostal artery; 2) the superior bronchial artery on the left side
A pulmonary consolidation is a region of normally compressible lung tissue that has filled with liquid instead of air. [1] The condition is marked by induration [2] (swelling or hardening of normally soft tissue) of a normally aerated lung.
For formation of BALT in mice is necessary inteleukin-17 and VCAM-1, PNAd and LFA-1 and it is lymphotoxin-α independent whereas the development of secondary lymphoid organs (such as lymph nodes and Peyer’s patches) is typically dependent on LTα. [4] [5] [6] Formation of BALT may be caused by disabled in situ function of Treg cells. [7]