6. Respiratory tract IS

B. The respiratory system not only mediates gas exchange but also conditions and filters inspired air, contributes to vocalization, detects odors, and helps regulate immune responses to inhaled antigens.

A.

E.

A.

B.

D.

No both are not, later days they believed lower to be

Respiratory bronchioles

B. Alveoli are terminal respiratory units clustered in alveolar sacs, connected to respiratory bronchioles by alveolar ducts, and serve as the primary site of gas exchange.

A

Because:

1. The nasal cavity and conducting airways filter large particles (>5 µm) via impaction and mucociliary clearance.

2. Smaller particles (1–5 µm) settle deeper by sedimentation in bronchioles.

3. Ultrafine particles (<1 µm) may reach the alveoli, where diffusion dominates due to low airflow velocity. → Thus, particle size decreases with progression down the conduction zones.

C. Oropharynx

• mucus

• anti microbial peptides

• epithelial barrier

goblet cells & mucus-secreting glands

1. Ciliated columnar cells

   • provide coordinated sweeping motion of the mucus

   • function as a mucocilary escelator

2. Airway basal cells

   • stem cell that differtiate into al epithelial cells type above bronchioles

1. goblet cells

   • produce mucins

1. club cells

   • producse antimicorbial factors

   • secretory cells appear in bronchioles & increase in number as goblet cells decrease

1. brush cells (tuft cells)

   • sensory & chemoreceptor cells

   • promote basal airway reflexes

   • basal surface from a synapse with an afferent nerve ending

2. pulmonary endocrine cells

   • respond to oxygen, stretch and chemical stimuli

   • 
     

-> terminal air spaces & site of gas exchange between air and blood

1. type 1 alveolar cells

   • facilitate gas exchange

   • no cell division

   • 40% but covr 95 % of aveoli surface

2. type 2 alveolar cells

   • 60 % onlx 5% surface

   • secretory cells od srufactants -> resuce surface tension at air and epithelium interface

NALT -> upper

iBALT -> lower

A. In humans, nasal-associated lymphoid tissue (NALT) forms part of Waldeyer’s ring, including tonsils and adenoids, while in the deeper lungs, inducible bronchus-associated lymphoid tissue (iBALT) forms only after antigenic stimulation.

• Location: Upper airways; part of Waldeyer’s ring (tonsils + adenoids).

• Structure: Permanent, well-organized secondary lymphoid tissue with distinct B- and T-cell zones.

• B cells: Form follicles and germinal centers → differentiate into IgA-producing plasma cells for mucosal defense.

• T cells: Mostly CD4⁺ helper cells supporting class switching to IgA and maintaining mucosal memory.

• Blood vessels: Rich in high endothelial venules (HEVs) → allow naive lymphocytes from the bloodstream to enter NALT.

• Lymphatic drainage: Connects to cervical lymph nodes, enabling immune-cell recirculation.

• Function: Constant immune surveillance against inhaled pathogens and antigens.

1. Location: In the lung parenchyma and around bronchi; forms only after inflammation or infection.

2. Structure: Inducible and less organized than NALT; develops de novo around small airways.

3. B cells: Form temporary follicles with germinal centers → produce IgA and IgG locally.

4. T cells: Include effector and memory subsets (CD4⁺ & CD8⁺) that can be activated locally.

5. Blood vessels: Develop new vessels resembling HEVs during inflammation → enable lymphocyte recruitment from blood.

6. Lymphatic vessels: Form alongside to allow antigen and cell drainage to lung-draining lymph nodes.

7. Function: Provides localized, rapid immune responses in lung tissue after antigen exposure.

NALT and lung-draining lymph nodes are the main secondary lymphoid sites where T and B cells are activated and differentiate into memory cells after encountering inhaled antigens.

1. From the nose: → The dendritic cell migrates to NALT (part of Waldeyer’s ring), where it presents the antigen to naive T and B cellsand initiates adaptive immune responses. → Some antigen-loaded dendritic cells may also traffic to cervical lymph nodes via lymphatic drainage.

2. From the lung: → The dendritic cell migrates to the regional lung-draining lymph nodes, mainly the hilar and mediastinal lymph nodes. → There, it activates T helper cells, which in turn help B cells undergo class-switching (often to IgA) and memory formation. → If iBALT is present (after infection), dendritic cells can also present antigen locally in the lung tissue.

alveolar macrophages

-> support epitheal inegrity

-> clear senescemt cells and inhaled antigens

Interstital macrophages

-> support stroma and T cells by production of IL-10

->

1. Inflammation: Alveolar macrophages activate and recruit monocytes → become proinflammatory macrophages (release TNF-α, IL-1β, IL-6).

2. Resolution: Macrophages switch to anti-inflammatory, reparative phenotype → clear apoptotic cells and secrete IL-10, TGF-β, resolvins.

3. Result: Inflammation ends, tissue heals, homeostasis restored.

1. upper airway inflammation,

2. lower airway homeostasis

3. upper airway homeostasis

4. lower airway inflammation

intra-epohtelia: CD8

lampina propria: CD4

• macrophages

• Treg

Through Tregs, anti-inflammatory macrophages, and epithelial-derived signals (IL-10, TGF-β) that limit immune activation against harmless antigens.

Neurons and immune cells communicate via neuropeptides and cytokines, coordinating inflammation, mucus secretion, and airway reflexes.

The stepwise decrease in O₂ pressure from inhaled air to tissues; ensures oxygen delivery for metabolism and immune function.

Via HIF-1α, hypoxia promotes proinflammatory Th17 and effector T-cell activity, while reducing Treg function, enhancing inflammation.