加熱黄砂によってもアレルギー炎症の増悪が認められることから、粒子自身の物理的刺激や、その主成分である二酸化ケイ素がアレルギーの増悪に係っているものと考えられる。図(3)-2 に肺胞洗浄液中のマクロファージ、好中球、好酸球等の炎症細胞を活性化する炎症性サイトカイン・ケモカインを示した。これらの炎症性サイトカイン・ケモカインの値は肺洗浄液中の炎症細胞数とパラレルであった。アレルギー炎症の主役である好酸球の遊走・活性化にあずかる IL-5（表(3)-3）や Eotaxin, MCP-3（表(3)-4）は OVA+非加熱黄砂（AASD）群で相乗的に増加し、好酸球数とよく対応していた。また好中球を遊走・活性化する KC や MIP-1α は非加熱黄砂単独投与によっても増加しており、これに伴って好中球の増加も認められた。

表(3)-3 肺洗浄液中 (BALF) のサイトカイン発現

Group*	Animals(n)	Cytokines (pg protein/total BALF)
IL-1 $ \beta $	IL-4	IL-5	IL-6	IL-12	IL-13
Control	8	11.1 ± 7.64	ND	ND	2.94 ± 1.81	6.71 ± 6.71	ND
H-AASD	8	50.7 ± 12.2	ND	2.39 ± 2.39	57.5 ± 19.1	311 ± 35.5	ND
AASD	8	245 ± 32.6 $ ^{\S} $	ND	6.76 ± 6.76	176 ± 21.4 $ ^{\S} $	693 ± 59.0 $ ^{\ddagger} $	3.38 ± 3.38
OVA	8	ND	ND	22.3 ± 6.67	1.82 ± 1.10	27.0 ± 14.3	ND
OVA + H-AASD	8	111 ± 34.9 $ ^{\dagger\dagger\dagger} $	ND	152 ± 20.1 $ ^{\ddagger\ddagger\ddagger} $	70.1 ± 18.4 $ ^{\dagger\dagger\dagger} $	467 ± 41.1	74.8 ± 17.2 $ 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ND: not detectable. Data were shown $ M \pm SE $

$$ {}_{p}^{\dagger}<0.05vs.Control, $$

$$ {}_{p}^{\ddagger}<0.01vs. $$

$$ 十十 p<0.001vs.OVA, $$

$$ ^{II}p<0.05vs.OVA, $$

$$ \mathrm{m m}_{p<0.01\mathrm{v s.~A A S D,}} $$

$$ ^{**}p<0.01vs.OVA, $$

$$ ^{***}p<0.001vs.AASD $$

表(3)-4 肺洗浄液中 (BALF) のケモカイン発現

Group*	Animals(n)	Chemokines (pg protein/total BALF)
RANTES	KC	MIP-1 $ \alpha $	Eotaxin	MCP-1	MCP-3
Control	8	ND	31.6 ± 12.5	ND	ND	ND	ND
H-AASD	8	13.5 ± 9.75	593 ± 89.0 $ ^{\dagger} $	62.1 ± 7.29 $ ^{\dagger} $	ND	267 ± 58.5	3.98 ± 3.98
AASD	8	73.0 ± 16.2 $ ^{\dagger} $	517 ± 63.1 $ ^{\dagger} $	62.9 ± 4.31 $ ^{\dagger} $	ND	342 ± 83.8	47.2 ± 24.6
OVA	8	ND	80.8 ± 18.7	ND	ND	ND	4.13 ± 4.13
OVA + H-AASD	8	16.9 ± 6.03	419 ± 32.9 $ ^{\ddagger\ddagger} $	13.5 ± 4.11 $ ^{\dagger\dagger} $	12.0 ± 6.11	1132 ± 302 $ ^{\dagger\S\ast\ast} $	396 ± 165
OVA + AASD	8	77.1 ± 23.8 $ ^{\dagger\S} $	583 ± 56.2 $ ^{\ddagger\ddagger} $	21.7 ± 2.61 $ ^{\dagger\S\ddagger\ddagger} $	45.9 ± 15.4 $ ^{\dagger\ddagger\ddagger\ddagger} $	1771 ± 340 $ ^{\dagger\ddagger\ddagger\ddagger} $	1012 ± 224 $ ^{\dagger\ddagger\ddagger\ddagger} $

All values were expressed as mean ± SE (n = 8). ND: not detectable.

$ ^{\dagger}p<0.01 $ vs. control, $ ^{\ddagger}p<0.001 $ vs. control, $ ^{\S}p<0.01 $ vs. OVA, $ ^{\parallel}p<0.001 $ vs. OVA,

$ ^{**}p<0.05 $ vs. H-AASD, $ \dagger\dagger\dagger p<0.001 $ vs. H-AASD, $ \ddagger\ddagger p<0.001 $ vs. AASD

図(3)-3 は肺の病理組織学的変化を示した。加熱黄砂群（図(3)-3B）では殆ど影響が見られないが、非加熱黄砂群（図(3)-3C）では気道周囲に炎症細胞が見られ、いわゆる気管支炎の病態が認められた。OVA 投与群（図(3)-3D）では軽度の気道上皮細胞の粘液細胞化と気道周囲にリンパ球等の炎症細胞浸潤が認められたが、OVA+加熱黄砂群、OVA+非加熱黄砂群ではこれらの変化が強く見られ、特に OVA+非加熱黄砂群（図(3)-3F）で著し変化が観察された。このような OVA+非加熱黄砂群で見られた喘息様病態の増悪は炎症性サイトカインやケモカインの相乗的増加によって引